1
40
25
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.jep.2006.12.015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jep.2006.12.015</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
458-463
Issue
3
Volume
111
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Dublin Core
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Title
A name given to the resource
Protective Effects Of Ginsenoside Rg(2) Against Glutamate-induced Neurotoxicity In Pc12 Cells
Publisher
An entity responsible for making the resource available
Journal of Ethnopharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-05
Subject
The topic of the resource
Alzheimer's disease; apoptosis; beta peptide; calpain; damage; excitotoxicity; expression; Integrative & Complementary; ischemic neuronal death; Medicine; neuroprotection; nitric-oxide; Panax ginseng; Panax ginseng; Pharmacology & Pharmacy; Plant Sciences; receptors; system
Creator
An entity primarily responsible for making the resource
Li N; Liu B; Dluzen D E; Jin Y
Description
An account of the resource
We investigated the effect of ginsenoside Rg(2) on neurotoxic activities induced by glutamate in PC12 cells. The cells were incubated with glutamate (1 mmol/L), glutamate and ginsenoside Rg(2) (0.05, 0.1, 0.2 mmol/L) or nimodipine (5 mu mol/L for 24 h. The cellular viability was assessed by MTT assay. The lipid peroxidation products malondialdehyde (MDA) and nitrogen oxide (NO) were measured by a spectrophotometric method. Fura2/AM, as a cell permeable fluorescent probe for Ca2+, was used to detect intracellular Ca2+ concentration ([Ca2+](i)) using a monespectrofluorometer. Immunocytochemical techniques were employed to check the protein expression levels of calpain II, caspase-3 and beta-amyloid (A beta)1-40 in PC12 cells. The results showed that glutamate decreased the cell viability, increased [Ca2+](i), lipid peroxidation (the excessive production of MDA, NO) and the protein expression levels of calpain II, caspase-3 and A beta 1-40 in PC12 cells. Ginsenoside Rg(2) significantly attenuated glutamate-induced neurotoxic effects upon these parameters at all doses tested. Our study suggests that ginsenoside Rg(2) has a neuroprotective effect against glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis. In addition, the inhibitory effect of ginsenoside Rg(2) against the formation of A beta 1-40 suggests that ginsenoside Rg(2) may also represent a potential treatment strategy for Alzheimer's disease. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jep.2006.12.015" target="_blank" rel="noreferrer noopener">10.1016/j.jep.2006.12.015</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2007
Alzheimer's disease
Apoptosis
beta peptide
calpain
damage
Dluzen D E
excitotoxicity
expression
Integrative & Complementary
ischemic neuronal death
Jin Y
Journal Article or Conference Abstract Publication
Journal of Ethnopharmacology
Li N
Liu B
Medicine
Neuroprotection
nitric-oxide
Panax ginseng
Pharmacology & Pharmacy
Plant Sciences
Receptors
system
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/pmic.200500447" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/pmic.200500447</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1250-1260
Issue
4
Volume
6
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Title
A name given to the resource
Increased Oxidation And Degradation Of Cytosolic Proteins In Alcohol-exposed Mouse Liver And Hepatoma Cells
Publisher
An entity responsible for making the resource available
Proteomics
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-02
Subject
The topic of the resource
alcoholism; apoptosis; Biochemistry & Molecular Biology; CYP2E1; cytochrome p-4502e1; Degradation; disease; ethanol; in-vitro; induced; injury; nitric-oxide; oxidative stress; oxidized proteins; peroxiredoxin; protein; protein oxidation; rat-liver; stress
Creator
An entity primarily responsible for making the resource
Kim B J; Hood B L; Aragon R A; Hardwick Jr; Conrads T R; Veenstra T D; Song B J
Description
An account of the resource
We recently developed a sensitive method using biotin-N-maleimide (biotin-NM) as a probe to positively identify oxidized mitochondrial proteins. In this study, biotin-NM was used to identify oxidized cytosolic proteins in alcohol-fed mouse livers. Alcohol treatment for 6 wk elevated the levels of CYP2E1 and nitrotyrosine, a marker of oxidative stress. Markedly increased levels of oxidized proteins were detected in alcohol-fed mouse livers compared to pair-fed controls. The biotin-NM-labeled oxidized proteins from alcohol-exposed mouse livers were subsequently purified with streptavidin-agarose and resolved on 2-DE. More than 90 silver-stained protein spots that displayed differential intensities on 2-D gels were identified by MS. Peptide sequence analysis revealed that many enzymes or proteins involved in stress response, chaperone activity, intermediary metabolism, and antioxidant defense systems such as peroxiredoxin were oxidized after alcohol treatment. Smaller fragments of many proteins were repeatedly detected only in alcohol-fed mice, indicating that many oxidized proteins after alcohol exposure were degraded. Immunoblot results showed that the level of oxidized peroxiredoxin (inactivated) was markedly increased in the alcohol-exposed mouse livers and ethanol-sensitive hepatoma cells compared to the corresponding controls. Our results may explain the underlying mechanism for cellular dysfunction and increased susceptibility to other toxic agents following alcohol-mediated oxidative stress.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/pmic.200500447" target="_blank" rel="noreferrer noopener">10.1002/pmic.200500447</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2006
alcoholism
Apoptosis
Aragon R A
Biochemistry & Molecular Biology
Conrads T R
CYP2E1
cytochrome p-4502e1
degradation
Disease
ETHANOL
Hardwick Jr
Hood B L
in-vitro
Induced
Injury
Journal Article or Conference Abstract Publication
Kim B J
nitric-oxide
Oxidative Stress
oxidized proteins
peroxiredoxin
Protein
Protein oxidation
proteomics
rat-liver
Song B J
Stress
Veenstra T D
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1126/scisignal.2003948" target="_blank" rel="noreferrer noopener">http://doi.org/10.1126/scisignal.2003948</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
12-12
Issue
287
Volume
6
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Dublin Core
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Title
A name given to the resource
Interference With Akt Signaling Protects Against Myocardial Infarction And Death By Limiting The Consequences Of Oxidative Stress
Publisher
An entity responsible for making the resource available
Science Signaling
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
adhesion molecule-1 expression; Biochemistry & Molecular Biology; cardiac dysfunction; Cell Biology; density-lipoprotein; extends life-span; foam cell-formation; nf-kappa-b; nitric-oxide; oxidized phospholipids; scavenger receptor cd36; sr-bi
Creator
An entity primarily responsible for making the resource
Kerr B A; Ma L N; West X Z; Ding L; Malinin N L; Weber M E; Tischenko M; Goc A; Somanath P R; Penn M S; Podrez E A; Byzova T V
Description
An account of the resource
The intricacy of multiple feedback loops in the pathways downstream of Akt allows this kinase to control multiple cellular processes in the cardiovascular system and precludes inferring consequences of its activation in specific pathological conditions. Akt1, the major Akt isoform in the heart and vasculature, has a protective role in the endothelium during atherosclerosis. However, Akt1 activation may also have detrimental consequences in the cardiovascular system. Mice lacking both the high-density lipoprotein receptor SR-BI (scavenger receptor class B type I) and ApoE (apolipoprotein E), which promotes clearance of remnant lipoproteins, are a model of severe dyslipidemia and spontaneous myocardial infarction. We found that Akt1 was activated in these mice, and this activation correlated with cardiac dysfunction, hypertrophy, and fibrosis; increased infarct area; cholesterol accumulation in macrophages and atherosclerosis; and reduced life span. Akt1 activation was associated with inflammation, oxidative stress, accumulation of oxidized lipids, and increased abundance of CD36, a major sensor of oxidative stress, and these events created a positive feedback loop that exacerbated the consequences of oxidative stress. Genetic deletion of Akt1 in this mouse model resulted in decreased mortality, alleviation of multiple complications of heart disease, and reduced occurrence of spontaneous myocardial infarction. Thus, interference with Akt1 signaling in vivo could be protective and improve survival under dyslipidemic conditions by reducing oxidative stress and responses to oxidized lipids.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1126/scisignal.2003948" target="_blank" rel="noreferrer noopener">10.1126/scisignal.2003948</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
adhesion molecule-1 expression
Biochemistry & Molecular Biology
Byzova T V
cardiac dysfunction
Cell Biology
density-lipoprotein
Ding L
extends life-span
foam cell-formation
Goc A
Journal Article or Conference Abstract Publication
Kerr B A
Ma L N
Malinin N L
nf-kappa-b
nitric-oxide
oxidized phospholipids
Penn M S
Podrez E A
scavenger receptor cd36
Science Signaling
Somanath P R
sr-bi
Tischenko M
Weber M E
West X Z
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/cmdc.201100559" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cmdc.201100559</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
375-384
Issue
3
Volume
7
Search for Full-text
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Dublin Core
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Title
A name given to the resource
Polycyclic Cage Structures As Lipophilic Scaffolds For Neuroactive Drugs
Publisher
An entity responsible for making the resource available
Chemmedchem
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-03
Subject
The topic of the resource
Alzheimer's disease; apoptosis; benzodiazepine-receptors; biological activity; cage compounds; calcium-antagonists; carbonic-anhydrase inhibitors; d-aspartate receptor; drug design; fluorescent ligands; monoamine-oxidase-b; neuroprotection; nitric-oxide; parkinsons-disease; Pharmacology & Pharmacy; sigma-receptors
Creator
An entity primarily responsible for making the resource
Joubert J; Geldenhuys W J; Van der Schyf C J; Oliver D W; Kruger H G; Govender T; Malan S F
Description
An account of the resource
Polycyclic cage scaffolds have been successfully used in the development of numerous lead compounds demonstrating activity in the central nervous system (CNS). Several neurodegenerative diseases, such as Alzheimers disease, Parkinsons disease, Huntingtons disease, schizophrenia, and stroke, as well as drug abuse, can be modulated with polycyclic cage derivatives. These cage moieties, including adamantane and pentacycloundecane derivatives, improve the pharmacokinetic and pharmacodynamic properties of conjugated parent drugs and serve as an important scaffold in the design of therapeutically active agents for the treatment of neurological disorders. In this Minireview, we focus on the recent developments in the field of polycyclic cage compounds, as well as the relationship between the lipophilic character of these cage-derived drugs and the ability of such compounds to target and reach the CNS and improve the pharmacodynamic properties of compounds conjugated to it.
Identifier
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<a href="http://doi.org/10.1002/cmdc.201100559" target="_blank" rel="noreferrer noopener">10.1002/cmdc.201100559</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Alzheimer's disease
Apoptosis
benzodiazepine-receptors
biological activity
cage compounds
calcium-antagonists
carbonic-anhydrase inhibitors
Chemmedchem
d-aspartate receptor
Drug Design
fluorescent ligands
Geldenhuys W J
Govender T
Joubert J
Journal Article or Conference Abstract Publication
Kruger H G
Malan S F
monoamine-oxidase-b
Neuroprotection
nitric-oxide
Oliver D W
parkinsons-disease
Pharmacology & Pharmacy
sigma-receptors
Van der Schyf C J
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.brainres.2004.10.004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2004.10.004</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
172-182
Issue
2
Volume
1030
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Title
A name given to the resource
Characterization Of Regional Cerebral Blood Flow And Expression Of Angiogenic Growth Factors In The Frontal Cortex Of Juvenile Male Shrsp And Shr
Publisher
An entity responsible for making the resource available
Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
2004-12
Subject
The topic of the resource
abnormalities; AD/HD; angiogemic factor; animal-model; attention-deficit/hyperactivity; brain; children; deficit-hyperactivity-disorder; disorder; frontal cortex; Neurosciences & Neurology; nitric-oxide; NOS isoform; regional cerebral blood flow; spontaneously hypertensive-rats; stroke-prone; vegf
Creator
An entity primarily responsible for making the resource
Jesmin S; Togashi H; Mowa C N; Ueno K; Yamaguchi T; Shibayama A; Miyauchi T; Sakuma I; Yoshioka M
Description
An account of the resource
Attention-deficit/hyperactivity disorder (AD/HD) is a common pediatric behavioral disorder associated with male preponderance and reduction of regional cerebral blood flow (rCBF). However, lack of an appropriate animal model exhibiting appropriate AD/HD symptoms stands in the way of studying mechanism(s) underlying reduced rCBF and male preponderance. Our group has been investigating the suitability of juvenile male stroke-prone spontaneously hypertensive rats (SHRSP), a substrain of the commonly used AD/HD animal model SHR, as a model for AD/HD because, unlike SHR, SHRSP displays cognitive impairment and male preponderance. Our more recent studies revealed alterations in the synthesis of sex steroid hormones and angiogenic factors in the frontal cortex of male SHRSP compared to the genetic control WKY. Based on these observations, the present study utilizes laser-Doppler flowmetry, histochemistry, enzyme immunoassay, immunoblotting, and real-time PCR to characterize and compare the patterns of regional cerebral blood flow and synthesis of angiogenic molecules [basic fibroblast growth factor; nitric oxide synthase isoforms (endothelial, neuronal and inducible); vascular endothelial growth factor (VEGF) and its signaling molecules VEGF receptors, phosphorylated Akt, endothelial nitric oxide synthase eNOS] between male SHRSP and SHR. Overall, consistent with our previous data showing alteration in VEGF/Akt/NO signaling, there was a marked reduction in the profile of rCBF (35%) and angiogenic factors of SHRSP, compared to age-matched genetic control Wistar-Kyoto rats (WKY) and SHR. We conclude that, unlike SHR, the profiles of rCBF and angiogenic factors in SHRSP are altered in juvenile male. Thus, SHRSP appears to be a more suitable animal model for studying changes in rCBF in AD/HD. (C) 2004 Elsevier B.V. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.brainres.2004.10.004" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2004.10.004</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2004
Abnormalities
AD/HD
angiogemic factor
animal-model
attention-deficit/hyperactivity
Brain
Brain research
Children
deficit-hyperactivity-disorder
disorder
frontal cortex
Jesmin S
Journal Article or Conference Abstract Publication
Miyauchi T
Mowa C N
Neurosciences & Neurology
nitric-oxide
NOS isoform
regional cerebral blood flow
Sakuma I
Shibayama A
spontaneously hypertensive-rats
stroke-prone
Togashi H
Ueno K
vegf
Yamaguchi T
Yoshioka M
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0065389" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0065389</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
17-17
Issue
6
Volume
8
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Alpha-lipoic Acid Antioxidant Treatment Limits Glaucoma-related Retinal Ganglion Cell Death And Dysfunction
Publisher
An entity responsible for making the resource available
Plos One
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-06
Subject
The topic of the resource
controlled trial aladin; dba/2j mouse model; glycation end-products; in-vivo; ischemia-reperfusion; nitric-oxide; open-angle glaucoma; optic neuropathy; oxidative stress; Science & Technology - Other Topics; trabecular meshwork
Creator
An entity primarily responsible for making the resource
Inman D M; Lambert W S; Calkins D J; Horner P J
Description
An account of the resource
Oxidative stress has been implicated in neurodegenerative diseases, including glaucoma. However, due to the lack of clinically relevant models and expense of long-term testing, few studies have modeled antioxidant therapy for prevention of neurodegeneration. We investigated the contribution of oxidative stress to the pathogenesis of glaucoma in the DBA/2J mouse model of glaucoma. Similar to other neurodegenerative diseases, we observed lipid peroxidation and upregulation of oxidative stress-related mRNA and protein in DBA/2J retina. To test the role of oxidative stress in disease progression, we chose to deliver the naturally occurring, antioxidant alpha-lipoic acid (ALA) to DBA/2J mice in their diet. We used two paradigms for ALA delivery: an intervention paradigm in which DBA/2J mice at 6 months of age received ALA in order to intervene in glaucoma development, and a prevention paradigm in which DBA/2J mice were raised on a diet supplemented with ALA, with the goal of preventing glaucoma development. At 10 and 12 months of age (after 4 and 11 months of dietary ALA respectively), we measured changes in genes and proteins related to oxidative stress, retinal ganglion cell (RGC) number, axon transport, and axon number and integrity. Both ALA treatment paradigms showed increased antioxidant gene and protein expression, increased protection of RGCs and improved retrograde transport compared to control. Measures of lipid peroxidation, protein nitrosylation, and DNA oxidation in retina verified decreased oxidative stress in the prevention and intervention paradigms. These data demonstrate the utility of dietary therapy for reducing oxidative stress and improving RGC survival in glaucoma.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0065389" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0065389</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
Calkins D J
controlled trial aladin
dba/2j mouse model
Department of Pharmaceutical Sciences
glycation end-products
Horner P J
in-vivo
Inman D M
ischemia-reperfusion
Journal Article or Conference Abstract Publication
Lambert W S
NEOMED College of Pharmacy
nitric-oxide
open-angle glaucoma
optic neuropathy
Oxidative Stress
PloS one
Science & Technology - Other Topics
trabecular meshwork
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.2174/1381612811319130004" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1381612811319130004</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2366-2374
Issue
13
Volume
19
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Microvascular Function/dysfunction Downstream A Coronary Stenosis
Publisher
An entity responsible for making the resource available
Current Pharmaceutical Design
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-04
Subject
The topic of the resource
artery disease; blood-flow; ca2+-activated k+ channels; Coronary microcirculation; coronary stenosis; endothelial dysfunction; flow-induced dilation; function; iib/iiia receptor blockade; left-ventricular wall; myocardial ischemia; myocardial-perfusion; nitric-oxide; Pharmacology & Pharmacy; resistive vessel; unstable angina
Creator
An entity primarily responsible for making the resource
Guarini G; Capozza P G; Huqi A; Morrone D; Chilian W M; Marzilli M
Description
An account of the resource
For decades coronary macrovascular atherosclerosis has been considered the principal manifestation of coronary heart disease, with most of our effort dedicated to identifying and removal of coronary stenosis. However, growing body of literature indicates that coronary microcirculation also contributes substantially to the pathophysiology of cardiovascular disease. An understanding of mechanisms regulating microvascular function is of critical importance in understanding its role in disease, especially because these regulatory mechanisms vary substantially across species, vascular bed and due to comorbidities. Indeed, the most obvious consequence of coronary stenosis is that it may limit blood supply to the dependent myocardium to the point of causing ischaemia during exercise or even at rest. However, this flow limiting effect is not only due to the passive hydraulic effect of a narrowed conduit, but also to active responses in the coronary microcirculation triggered by the presence of an epicardial stenosis. To understand this problem it is important to review the inter-related mechanisms that regulate flow to the left ventricular wall and modulate transmural distribution of flow. These regulatory mechanisms operate hierarchically and are heterogeneously distributed along the coronary vascular tree. It is also important to discuss the effect of myocardial performance in modulating both blood flow demands and coronary resistance. Some of the interactions between coronary stenosis and microcirculation are transient, like those documented in acute coronary syndromes or during percutaneous interventions. However, microcirculatory remodeling may be triggered by a chronic coronary stenosis, leading to a sustained impairment of blood supply even after successful removal of the epicardial stenosis. A deeper understanding of these phenomena may explain paradoxical findings in patients undergoing coronary revascularization, particularly when functional tests are used in their assessment. These aspects are discussed in detail in this review.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.2174/1381612811319130004" target="_blank" rel="noreferrer noopener">10.2174/1381612811319130004</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
artery disease
blood-flow
ca2+-activated k+ channels
Capozza P G
Chilian W M
Coronary microcirculation
coronary stenosis
Current Pharmaceutical Design
endothelial dysfunction
flow-induced dilation
Function
Guarini G
Huqi A
iib/iiia receptor blockade
Journal Article or Conference Abstract Publication
left-ventricular wall
Marzilli M
Morrone D
myocardial ischemia
myocardial-perfusion
nitric-oxide
Pharmacology & Pharmacy
resistive vessel
unstable angina
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s00395-013-0387-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-013-0387-4</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
12-12
Issue
6
Volume
108
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Role Of Genetic Polymorphisms Of Ion Channels In The Pathophysiology Of Coronary Microvascular Dysfunction And Ischemic Heart Disease
Publisher
An entity responsible for making the resource available
Basic Research in Cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-11
Subject
The topic of the resource
artery-disease; atherosclerosis; Atrial fibrillation; Cardiovascular System & Cardiology; Coronary microcirculation; dysfunction; endothelial; Endothelium; gene; Genetic polymorphisms; Ion channels; Ischemic heart disease; k-atp channels; kir6.2; late sodium current; nitric-oxide; sensitive potassium channels; smooth-muscle; type-2 diabetes-mellitus; vascular
Creator
An entity primarily responsible for making the resource
Fedele F; Mancone M; Chilian W M; Severino P; Canali E; Logan S; De Marchis M L; Volterrani M; Palmirotta R; Guadagni F
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-013-0387-4" target="_blank" rel="noreferrer noopener">10.1007/s00395-013-0387-4</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
artery-disease
Atherosclerosis
Atrial fibrillation
Basic research in cardiology
Canali E
Cardiovascular System & Cardiology
Chilian W M
Coronary microcirculation
De Marchis M L
dysfunction
Endothelial
Endothelium
Fedele F
gene
Genetic polymorphisms
Guadagni F
Ion Channels
Ischemic heart disease
k-atp channels
kir6.2
late sodium current
Logan S
Mancone M
nitric-oxide
Palmirotta R
sensitive potassium channels
Severino P
smooth-muscle
type-2 diabetes-mellitus
Vascular
Volterrani M
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/j.1365-2362.2007.01779.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1365-2362.2007.01779.x</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
222-230
Issue
3
Volume
37
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Bile Synthesis In Rat Models Of Inflammatory Bowel Diseases
Publisher
An entity responsible for making the resource available
European Journal of Clinical Investigation
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-03
Subject
The topic of the resource
acid synthesis; acute-phase response; acute-phase response; bile synthesis; cholesterol 7-alpha hydroxylase; cholesterol 7-alpha-hydroxylase gene; colitis; crohns-disease; experimental; General & Internal Medicine; inflammatory bowel disease; intestinal inflammation; messenger-rna; nitric-oxide; Research & Experimental Medicine; sulfonic-acid; ulcerative-colitis
Creator
An entity primarily responsible for making the resource
Dikopoulos N; Schmid R M; Bachem M; Buttenschoen K; Adler G; Chiang J Y L; Weidenbach H
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1365-2362.2007.01779.x" target="_blank" rel="noreferrer noopener">10.1111/j.1365-2362.2007.01779.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2007
acid synthesis
acute-phase response
Adler G
Bachem M
bile synthesis
Buttenschoen K
Chiang J Y L
cholesterol 7-alpha hydroxylase
cholesterol 7-alpha-hydroxylase gene
Colitis
crohns-disease
Dikopoulos N
European Journal of Clinical Investigation
Experimental
General & Internal Medicine
inflammatory bowel disease
intestinal inflammation
messenger-rna
nitric-oxide
Research & Experimental Medicine
Schmid R M
sulfonic-acid
ulcerative-colitis
Weidenbach H
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.yjmcc.2011.10.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2011.10.001</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
794-801
Issue
4
Volume
52
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mechanisms Of Metabolic Coronary Flow Regulation
Publisher
An entity responsible for making the resource available
Journal of Molecular and Cellular Cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-04
Subject
The topic of the resource
Adenosine; arteriolar; Carbon dioxide; Cardiovascular System & Cardiology; Cell Biology; Coronary blood flow; dilation; guinea-pig heart; heterogeneity; hydrogen-peroxide; hypercapnic acidosis; Ion channels; k-atp channels; microvascular dilation; myocardial blood-flow; nitric-oxide; nitric-oxide; Oxygen; Prostaglandins; Reactive oxygen species; sensitive potassium channels; spatial
Creator
An entity primarily responsible for making the resource
Deussen A; Ohanyan V; Jannasch A; Yin L Y; Chilian W
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yjmcc.2011.10.001" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2011.10.001</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
adenosine
arteriolar
Carbon Dioxide
Cardiovascular System & Cardiology
Cell Biology
Chilian W
Coronary blood flow
Deussen A
dilation
guinea-pig heart
heterogeneity
hydrogen-peroxide
hypercapnic acidosis
Ion Channels
Jannasch A
Journal of molecular and cellular cardiology
k-atp channels
microvascular dilation
myocardial blood-flow
nitric-oxide
Ohanyan V
Oxygen
Prostaglandins
reactive oxygen species
sensitive potassium channels
spatial
Yin L Y
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/hep.21372" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.21372</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1218-1230
Issue
5
Volume
44
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Inactivation of oxidized and S-nitrosylated mitochondrial proteins in alcoholic fatty liver of rats
Publisher
An entity responsible for making the resource available
Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006-11
Subject
The topic of the resource
oxidative stress; nitric-oxide; Gastroenterology & Hepatology; activated receptor-alpha; mouse-liver; Aldehyde dehydrogenase; cytochrome-p450 cyp2e1; dependent hepatotoxicity; ethanol-consumption; hepatic mitochondria; nitrosative stress
Creator
An entity primarily responsible for making the resource
Moon K H; Hood B L; Kim B J; Hardwick J P; Conrads T P; Veenstra T D; Song B Y J
Description
An account of the resource
Increased oxidative/nitrosative stress is a major contributing factor to alcohol-mediated mitochondrial dysfunction. However, which mitochondrial proteins are oxidatively modified under alcohol-induced oxidative/nitrosative stress is poorly understood. The aim of this study was to systematically investigate oxidized and/or S-nitrosylated mitochondrial proteins and to use a biotin-N-maleimide probe to evaluate their inactivation in alcoholic fatty livers of rats. Binge or chronic alcohol exposure significantly elevated nitric oxide, inducible nitric oxide synthase, and ethanol-inducible CYP21. The biotin-N-maleimide-labeled oxidized and/or S-nitrosylated mitochondrial proteins from pair-fed controls or alcohol-fed rat livers were subsequently purified with streptavidin-agarose. The overall patterns of oxidized and/or S-nitrosylated proteins resolved by 2-dimensional polyacrylamide gel electrophoresis were very similar in the chronic and binge alcohol treatment groups. Seventy-nine proteins that displayed differential spot intensities from those of control rats were identified by mass spectrometry. These include mitochondrial aldehyde dehydrogenase 2 (ALDH2), ATP synthase, acyl-CoA dehydrogenase, 3-ketoacyl-CoA thiolase, and many proteins involved in chaperone activity, mitochondrial electron transfer, and ion transport. The activity of 3-ketoacyl-CoA thiolase involved in mitochondrial beta-oxidation of fatty acids was significantly inhibited in alcohol-exposed rat livers, consistent with hepatic fat accumulation, as determined by biochemical and histological analyses. Measurement of activity and immunoblot results showed that ALDH2 and ATP synthase were also inhibited through oxidative modification of their cysteine or tyrosine residues in alcoholic fatty livers of rats. (In conclusion) under bar our results help to explain the underlying mechanism for mitochondrial dysfunction and increased susceptibility to alcohol-mediated liver damage.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.21372" target="_blank" rel="noreferrer noopener">10.1002/hep.21372</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2006
activated receptor-alpha
Aldehyde Dehydrogenase
Conrads T P
cytochrome-p450 cyp2e1
dependent hepatotoxicity
ethanol-consumption
Gastroenterology & Hepatology
Hardwick J P
hepatic mitochondria
Hepatology
Hood B L
Journal Article or Conference Abstract Publication
Kim B J
Moon K H
mouse-liver
nitric-oxide
nitrosative stress
Oxidative Stress
Song B Y J
Veenstra T D
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M109.056846" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M109.056846</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
3168-3180
Issue
5
Volume
285
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Peptide-based Antibodies against Glutathione-binding Domains Suppress Superoxide Production Mediated by Mitochondrial Complex I
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-01
Subject
The topic of the resource
oxidative stress; Biochemistry & Molecular Biology; nitric-oxide; proteins; site; generation; s-nitrosylation; postischemic heart; radical formation; bovine heart-mitochondria; nadh-ubiquinone oxidoreductase
Creator
An entity primarily responsible for making the resource
Chen J F; Chen C L; Rawale S; Chen C A; Zweier J L; Kaumaya P T P; Chen Y R
Description
An account of the resource
Complex I (NQR) is a critical site of superoxide (O-2(radical anion)) production and the major host of redox protein thiols in mitochondria. In response to oxidative stress, NQR-derived protein thiols at the 51- and 75-kDa subunits are known to be reversibly S-glutathionylated. Although several glutathionylated domains from NQR 51 and 75 kDa have been identified, their roles in the regulatory functions remain to be explored. To gain further insights into protein S-glutathionylation of complex I, we used two peptides of S-glutathionylated domain ((200)GAGAYI (C) under bar GEETALIESIEGK(219) of 51-kDa protein and (VDSDTL)-V-361 (C) under bar TEEVFPTAGAGTDLR(382) of 75-kDa protein) as chimeric epitopes incorporating a "promiscuous" T-cell epitope to generate two polyclonal antibodies, AbGSCA206 and AbGSCB367. Binding of AbGSCA206 and AbGSCB367 inhibited NQR-mediated O-2(radical anion). generation by 37 and 57%, as measured by EPR spin-trapping. To further provide an appropriate control, two peptides of non-glutathionylated domain ((21)SGDTTAPKKTSFGSLKDFDR(40) of 51-kDa peptide and (100)WNILTNSEKTKKAREGVMEFL(120) of 75-kDa peptide) were synthesized as chimeric epitopes to generate two polyclonal antibodies, Ab51 and Ab75. Binding of A51 did not affect NQR-mediated O-2(radical anion) generation to a significant level. However, binding of Ab75 inhibited NQR- mediated O-2(radical anion) generation by 35%. None of AbGSCA206, AbGSCB367, Ab51, or Ab75 showed an inhibitory effect on the electron transfer activity of NQR, suggesting that antibody binding to the glutathione-binding domain decreased electron leakage from the hydrophilic domain of NQR. When heart tissue homogenates were immunoprecipitated with Ab51 or Ab75 and probed with an antibody against glutathione, protein S-glutathionylation was enhanced in post-ischemic myocardium at the NQR 51-kDa subunit, but not at the 75-kDa subunit, indicating that the 51-kDa subunit of flavin subcomplex is more sensitive to oxidative stress resulting from myocardial infarction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M109.056846" target="_blank" rel="noreferrer noopener">10.1074/jbc.M109.056846</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
Biochemistry & Molecular Biology
bovine heart-mitochondria
Chen C A
Chen C L
Chen J F
Chen Y R
generation
Journal Article or Conference Abstract Publication
Journal of Biological Chemistry
Kaumaya P T P
nadh-ubiquinone oxidoreductase
nitric-oxide
Oxidative Stress
postischemic heart
Proteins
radical formation
Rawale S
s-nitrosylation
site
Zweier J L
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
806-812
Issue
10
Volume
77
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Role of angiotensin II in sympathetic nervous system induced left ventricular dysfunction
Publisher
An entity responsible for making the resource available
Canadian Journal of Physiology and Pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
1999
1999-10
Subject
The topic of the resource
contractility; Physiology; myocardium; Pharmacology & Pharmacy; nitric-oxide; catecholamines; inhibitors; mechanisms; hearts; rabbits; bradykinin; attenuation; calcium channel opener-blocker; captopril; converting-enzyme inhibitor; myocardial; nifedipine; ramiprilat
Creator
An entity primarily responsible for making the resource
Bosso F J; Jarjoura D G; Pilati C F
Description
An account of the resource
Experiments were undertaken to determine whether angiotensin (Ang) II concentration increases during massive sympathetic nervous system (SNS) activation and whether such an increase plays a role in the pathogenesis of SNS-induced left ventricular (LV) dysfunction. We also sought to determine whether excessive Ca2+ uptake through L-type channels due to intense adrenoceptor activation is responsible for the LV dysfunction. AngII concentration was measured in the plasma and myocardium before and after massively activating the SNS with an intracisternal injection of veratrine. In separate experiments, rabbits were given losartan, enalaprilat, enalaprilat plus HOE-140, nifedipine, betaBay K 4866, or saline before massively activating the SNS. LV function was evaluated 2.5 h later. The intense SNS activity caused plasma and myocardial AngII to increase by 400 and 437%, respectively. AngII receptor blockade did not prevent LV dysfunction. In contrast, enalaprilat reduced the degree of dysfunction, but its cardioprotection was abolished by HOE-140. Although nifedipine prevented SNS-induced LV dysfunction, administration of the Ca2+ channel opener, betaBay K 4866, did not increase its severity. Our results indicate that AngII is not involved in the pathogenesis of SNS-induced LV dysfunction and that the cardioprotection provided by angiotensin converting enzyme (ACE) inhibition is due to activation of a bradykinin pathway. Furthermore, the finding that the magnitude of the LV dysfunction was reduced by enalaprilat, and not increased by betaBay K 4866, suggests that intense adrenoceptor activation of L-type Ca2+ channels is not the primary pathogenetic mechanism.
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1999
attenuation
Bosso F J
bradykinin
calcium channel opener-blocker
Canadian journal of physiology and pharmacology
captopril
catecholamines
contractility
converting-enzyme inhibitor
hearts
inhibitors
Jarjoura D G
Journal Article or Conference Abstract Publication
mechanisms
myocardial
Myocardium
nifedipine
nitric-oxide
Pharmacology & Pharmacy
Physiology
Pilati C F
Rabbits
ramiprilat
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00876.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00876.2009</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
H966-H973
Issue
3
Volume
298
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome
Publisher
An entity responsible for making the resource available
American Journal of Physiology-Heart and Circulatory Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-03
Subject
The topic of the resource
exercise; Physiology; Cardiovascular System & Cardiology; nitric-oxide; blood flow; coronary blood flow; smooth-muscle-cells; insulin-resistance; cardiovascular-disease; pigs; ca2+-activated k+ channels; induced relaxation; Ossabaw miniature swine; A; diabetic dyslipidemic; exercising dogs; myocardial oxygen consumption; myocardial-metabolism; penitrem
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Payne G A; Payne B D; Svendsen M C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
Description
An account of the resource
Borbouse L, Dick GM, Payne GA, Payne BD, Svendsen MC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome. Am J Physiol Heart Circ Physiol 298: H966-H973, 2010. First published December 31, 2009; doi:10.1152/ajpheart.00876.2009.-This investigation was designed to examine the hypothesis that impaired function of coronary microvascular large-conductance Ca2+-activated K+ (BKCa) channels in metabolic syndrome (MetS) significantly attenuates the balance between myocardial oxygen delivery and metabolism at rest and during exercise-induced increases in myocardial oxygen consumption (M(V) over dotO(2)). Studies were conducted in conscious, chronically instrumented Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) that induces many common features of MetS. Data were collected under baseline/resting conditions and during graded treadmill exercise before and after selective blockade of BKCa channels with penitrem A (10 mu g/kg iv). We found that the exercise-induced increases in blood pressure were significantly elevated in MetS swine. No differences in baseline cardiac function or heart rate were noted. Induction of MetS produced a parallel downward shift in the relationship between coronary venous PO2 and M(V) over dotO(2) (P < 0.001) that was accompanied by a marked release of lactate (negative lactate uptake) as M(V) over dotO(2) was increased with exercise (P < 0.005). Inhibition of BKCa channels with penitrem A did not significantly affect blood pressure, heart rate, or the relationship between coronary venous PO2 and M(V) over dotO(2) in lean or MetS swine. These data indicate that BKCa channels are not required for local metabolic control of coronary blood flow under physiological (lean) or pathophysiological (MetS) conditions. Therefore, diminished function of BKCa channels does not contribute to the impairment of myocardial oxygen-supply demand balance in MetS.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00876.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00876.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
A
Alloosh M
American Journal of Physiology-Heart and Circulatory Physiology
blood flow
Borbouse L
Bratz I N
ca2+-activated k+ channels
Cardiovascular System & Cardiology
cardiovascular-disease
Coronary blood flow
diabetic dyslipidemic
Dick G M
Exercise
exercising dogs
induced relaxation
insulin-resistance
Journal Article or Conference Abstract Publication
myocardial oxygen consumption
myocardial-metabolism
Neeb Z P
nitric-oxide
Ossabaw miniature swine
Payne B D
Payne G A
penitrem
Physiology
pigs
smooth-muscle-cells
Sturek M
Svendsen M C
Tune J D
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2009.06.017" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2009.06.017</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
767-778
Issue
6
Volume
47
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Role of peroxisome proliferator-activated receptor-alpha in fasting-mediated oxidative stress
Publisher
An entity responsible for making the resource available
Free Radical Biology and Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-09
Subject
The topic of the resource
Aldehyde dehydrogenase; Biochemistry & Molecular Biology; differential expression; dismutase; Endocrinology & Metabolism; Fasting; fatty-acid oxidation; glutathione-s-transferase; hepatic steatosis; Lipid peroxidation; Lipid peroxidation; liver; manganese-superoxide-dismutase; mitochondrial aldehyde dehydrogenase; nitric-oxide; Null mice; oxidative stress; PPAR-alpha; PPAR-alpha; Protein nitration; Protein oxidation; rat-liver; Steatosis; Superoxide
Creator
An entity primarily responsible for making the resource
Abdelmegeed M A; Moon K H; Hardwick J P; Gonzalez F J; Song B J
Description
An account of the resource
The peroxisome proliferator-activated receptor-alpha (PPAR alpha) regulates lipid homeostasis, particularly in the liver. This study was aimed at elucidating the relationship between hepatosteatosis and oxidative stress during fasting. Fasted Ppara-null mice exhibited marked hepatosteatosis, which was associated with elevated levels of lipid peroxidation, nitric oxide synthase activity, and hydrogen peroxide accumulation. Total glutathione (GSH), mitochondrial GSH, and the activities of major antioxidant enzymes were also lower in the fasted Ppara-null mice. Consequently, the number and extent of nitrated proteins were markedly increased in the fasted Ppara-null mice, although high levels of protein nitration were still detected in the fed Ppara-null mice while many oxidatively modified proteins were only found in the fasted Ppara-null mice. However, the role of inflammation in increased oxidative stress in the fasted Ppara-null mice was minimal based on the similar levels of tumor necrosis factor-alpha change in all groups. These results with increased oxidative stress observed in the fasted Ppara-null mice compared with other groups demonstrate a role for PPAR alpha in fasting-mediated oxidative stress and that inhibition of PPAR alpha functions may increase the susceptibility to oxidative damage in the presence of another toxic agent. Published by Elsevier Inc.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2009.06.017" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2009.06.017</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
Abdelmegeed M A
Aldehyde Dehydrogenase
Biochemistry & Molecular Biology
differential expression
dismutase
Endocrinology & Metabolism
Fasting
fatty-acid oxidation
Free Radical Biology and Medicine
glutathione-s-transferase
Gonzalez F J
Hardwick J P
hepatic steatosis
Journal Article or Conference Abstract Publication
Lipid Peroxidation
Liver
manganese-superoxide-dismutase
mitochondrial aldehyde dehydrogenase
Moon K H
nitric-oxide
Null mice
Oxidative Stress
PPAR-alpha
Protein nitration
Protein oxidation
rat-liver
Song B J
Steatosis
superoxide
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
4307-4312
Issue
10
Volume
32
Search for Full-text
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Serum Folate: A Pharmacodynamic Biomarker of Intracellular Nitrosylcobalamin Activity Following Intravenous Administration in Dogs
Publisher
An entity responsible for making the resource available
Anticancer Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-10
Subject
The topic of the resource
apo2l/trail; biomarker; cells; cobalamin; disease; dogs; Folate; homocysteine; methylmalonic acid; nitric-oxide; Nitrosylcobalamin; Oncology; pharmacokinetics; supplementation; suppression; vitamin B-12; vitamin B-12
Creator
An entity primarily responsible for making the resource
Sysel A M; Horne W I; Steiner J M; Suchodolski J S; Bauer J A
Description
An account of the resource
Background/Aim: Cobalamin and folate are interdependent co-factors of the methionine synthase pathway. This study evaluated the effect of intravenously-administered nitrosylcobalamin (NO-Cbl), a vitamin B12 analog, on serum folate concentrations in healthy dogs. Materials and Methods: Four dogs received a 10-mg/kg, 20-mg/kg and 40-mg/kg intravenous bolus dose of NO-Cbl, with a 14-day washout period between doses. Blood samples were collected at baseline and post-dosing, and serum cobalamin and folate concentrations were measured. Results: For each dose, serum cobalamin concentrations were inversely correlated with serum folate concentrations. Spearman rank correlation coefficient values were -0.976 (10 mg/kg, p<0.0096), and -1.0 (20 mg/kg, p<0.008; 40 mg/kg, p<0.0046). Conclusion: Cellular uptake of NO-Cbl, following intravenous administration exerted a biological effect on folate similar to that previously described for other vitamin B12 analogs. Serum folate concentration may serve as a pharmacodynamic biomarker of intracellular nitrosylcobalamin activity following intravenous administration.
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2012
Anticancer research
apo2l/trail
Bauer J A
Biomarker
Cells
cobalamin
Disease
Dogs
Folate
homocysteine
Horne W I
Journal Article
methylmalonic acid
nitric-oxide
Nitrosylcobalamin
oncology
pharmacokinetics
Steiner J M
Suchodolski J S
supplementation
suppression
Sysel A M
vitamin B-12
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
3749-3752
Issue
9
Volume
32
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Pharmacokinetics of Intravenous Nitrosylcobalamin, an Antitumor Agent, in Healthy Beagle Dogs: A Pilot Study
Publisher
An entity responsible for making the resource available
Anticancer Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-09
Subject
The topic of the resource
apo2l/trail; canine organs; cobalamin; cobalamin vitamin-b-12; dogs; intravenous; nitric-oxide; Nitrosylcobalamin; Oncology; pharmacokinetics; protein; release; suppression; transcobalamin-ii; transport; vitamin B-12
Creator
An entity primarily responsible for making the resource
Sysel A M; Horne W I; Steiner J M; Suchodolski J S; Bauer J A
Description
An account of the resource
Background/Aim: Nitrosylcobalamin (NO-Cbl) is a cobalamin-based anti-tumor agent. This study evaluated the pharmacokinetic parameters of NO-Cbl following intravenous administration in dogs. Materials and Methods: Four dogs received 10 mg/kg, 20 mg/kg and 40 mg/kg intravenous bolus doses of NO-Cbl, with a 14-day washout period between doses. Blood samples were collected at baseline and post-dosing, and noncompartmental pharmacokinetic parameters were determined. Results: Average peak serum concentrations of 2265, 5523 and 13,866 pg/mL were achieved following single-dose bolus intravenous administration of 10 mg/kg, 20 mg/kg and 40 mg/kg of NO-Cbl respectively. The average area under the curve was 12,697 h x pg/mL, 24,497 h x pg/mL and 44,976 h x pg/mL respectively, with an average elimination half-life of 16.2 h, 13.5 h and 13.1 h respectively. Conclusion: These results can be used to determine the dose and dosing intervals for clinical trials evaluating NO-Cbl in humans and companion animals.
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2012
Anticancer research
apo2l/trail
Bauer J A
canine organs
cobalamin
cobalamin vitamin-b-12
Dogs
Horne W I
Intravenous
Journal Article
nitric-oxide
Nitrosylcobalamin
oncology
pharmacokinetics
Protein
release
Steiner J M
Suchodolski J S
suppression
Sysel A M
transcobalamin-ii
transport
vitamin B-12
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-1
Issue
21
Volume
126
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mitochondrial Transfer Restores Endothelial Dependent Vasodilation
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-11
Subject
The topic of the resource
blood-flow; Cardiovascular System & Cardiology; Endothelium; Mitochondria; nitric-oxide; Vascular disease
Creator
An entity primarily responsible for making the resource
Ohanyan V A; Kolz C L; Logan S; Yin L Y; Guarini G; Chen Y R; Chen C L; Pung Y F; Hardwick J P; Chilian W
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2012
blood-flow
Cardiovascular System & Cardiology
Chen C L
Chen Y R
Chilian W
Circulation
Endothelium
Guarini G
Hardwick J P
Journal Article
Kolz C L
Logan S
Mitochondria
nitric-oxide
Ohanyan V A
Pung Y F
Vascular disease
Yin L Y
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1021/bi9018237" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/bi9018237</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2529-2539
Issue
11
Volume
49
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Title
A name given to the resource
Peroxynitrite-Mediated Oxidative Modifications of Complex II: Relevance in Myocardial Infarction
Publisher
An entity responsible for making the resource available
Biochemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-03
Subject
The topic of the resource
Biochemistry & Molecular Biology; cytochrome-c; fatty-acids; identification; membrane; mitochondrial; modulation; nitric-oxide; postischemic heart; succinate-ubiquinone; thiyl
Creator
An entity primarily responsible for making the resource
Zhang L W; Chen C L; Kang P T; Garg V; Hu K L; Green-Church K B; Chen Y R
Description
An account of the resource
Increased O-2(center dot-) and NO production is a key mechanism of mitochondrial dysfunction in mycocardial ischemia/reperfusion injury. In complex impairment and enhanced tyrosine nitration of the 70 kDa FAD-binding protein occur in the post-ischemic myocardium and are thought to be mediated by peroxynitrite (OONO-) ill vivo [Chen, Y.-R., et ill. (2008) J. Biol. Chem. 283, 27991-28003]. To gain deeper insights into the redox protein thiols involved ill OONO--mediated Oxidative post-translational modifications relevant ill myocardial infarction, We subjected Isolated myocardial complex 11 to ill vltro protein nitration with OONO-. This resulted ill site-specific nitration at the 70 kDa polypeptide and impairment of complex II-derived electron transfer activity. Under reducing conditions, the gel band of the 70 kDa POlyPePtldC MIS subjected to in-gel trypsin/chymotrypsin digestion and then LC-MS/MS analysis Nitration Of Y-56 and Y-142 was previosly reported. Further analysis revealed that C-267, C-476 and C-537 are involved ill OONO--mediated S-sulfonation. To identify the disulfide formation mediated by OONO-, nitrated complex 11 was alkylated with iodoacetamide. In-gel proteolytic digestion and LC-MS/MS analysis were conducted under nonreducing conditions. The MS/MS data were examined with MassMatrix, indicating that three cysteine pairs, C-306-C-312,C-439-C-444, and C-288-C-575, were involved in OONO--mediated disulfide formation. Immuno-spin trapping with an anti-DMPO antibody and subsequent MS Was used to define Oxidative modification with protein radical formation. An OONO--dependent DMPO adduct was detected. and further LC-MS/MS analysis indicated C-288 and C-655 were involved in DMPO binding. These I-CSLIltS offered a complete profile of OONO--mediated Oxidative modifications that may be relevant Ill the disease model of myocardial infarction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1021/bi9018237" target="_blank" rel="noreferrer noopener">10.1021/bi9018237</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2010
BIOCHEMISTRY
Biochemistry & Molecular Biology
Chen C L
Chen Y R
cytochrome-c
fatty-acids
Garg V
Green-Church K B
Hu K L
identification
Journal Article
Kang P T
membrane
Mitochondrial
modulation
nitric-oxide
postischemic heart
succinate-ubiquinone
thiyl
Zhang L W
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s11517-008-0329-8" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11517-008-0329-8</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
433-442
Issue
5
Volume
46
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Chaotic behavior of the coronary circulation
Publisher
An entity responsible for making the resource available
Medical & Biological Engineering & Computing
Date
A point or period of time associated with an event in the lifecycle of the resource
2008
2008-05
Subject
The topic of the resource
adenosine concentration; blood-flow; chaos; Computer Science; Coronary circulation; Coronary microcirculation; dependent protein-kinase; dynamic-response; Engineering; exercise; k-atp(+) channels; Mathematical & Computational Biology; Medical Informatics; modeling; nitric; nitric-oxide; oxide; time-series; vascular-resistance; vasodilation
Creator
An entity primarily responsible for making the resource
Trzeciakowski J; Chilian W M
Description
An account of the resource
The regulation of the coronary circulation is a complex paradigm in which many inputs that influence vasomotor tone have to be integrated to provide the coronary vasomotor adjustments to cardiac metabolism and to perfusion pressure. We hypothesized that the integration of many disparate signals that influence membrane potential of smooth muscle cells, calcium sensitivity of contractile filaments, receptor trafficking result in complex non-linear characteristics of coronary vasomotion. To test this hypothesis, we measured an index of vasomotion, flowmotion, the periodic fluctuations of flow that reflect dynamic changes in resistances in the microcirculation. Flowmotion was continuously measured in periods ranging from 15 to 40 min under baseline conditions, during antagonism of NO synthesis, and during combined purinergic and NOS antagonism in the beating heart of anesthetized open-chest dogs. Flowmotion was measured in arterioles ranging from 80 to 135 mu m in diameter. The signals from the flowmotion measurements were used to derive quantitative indices of non-linear behavior: power spectra, chaotic attractors, correlation dimensions, and the sum of the Lyapunov exponents (Kolmogorov-Sinai entropy), which reflects the total chaos and unpredictability of flowmotion. Under basal conditions, the coronary circulation demonstrated chaotic non-linear behavior with a power spectra showing three principal frequencies in flowmotion. Blockade of nitric oxide synthase or antagonism of purinergic receptors did not affect the correlation dimensions, but significantly increased the Kolmogorov-Sinai entropy, altered the power spectra of flowmotion, and changed the nature of the chaotic attractor. These changes are consistent with the view that certain endogenous controls, nitric oxide and various purines (AMP, ADP, ATP, adenosine) make the coronary circulation more predictable, and that blockade of these controls makes the control of flow less predictable and more chaotic.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s11517-008-0329-8" target="_blank" rel="noreferrer noopener">10.1007/s11517-008-0329-8</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2008
adenosine concentration
blood-flow
chaos
Chilian W M
Computer Science
Coronary Circulation
Coronary microcirculation
dependent protein-kinase
dynamic-response
Engineering
Exercise
Journal Article
k-atp(+) channels
Mathematical & Computational Biology
Medical & Biological Engineering & Computing
Medical Informatics
modeling
nitric
nitric-oxide
oxide
time-series
Trzeciakowski J
vascular-resistance
vasodilation
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1021/ja904670x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/ja904670x</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
15078-+
Issue
42
Volume
131
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Vitamin B-12 and Redox Homeostasis: Cob(II)alamin Reacts with Superoxide at Rates Approaching Superoxide Dismutase (SOD)
Publisher
An entity responsible for making the resource available
Journal of the American Chemical Society
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-10
Subject
The topic of the resource
binding; chaperone; Chemistry; cobalamin; free-radicals; mechanism; nitric-oxide; oxidation; state
Creator
An entity primarily responsible for making the resource
Suarez-Moreira E; Yun J; Birch C S; Williams J H H; McCaddon A; Brascht N E
Description
An account of the resource
We report a kinetic study of the reaction between superoxide and an important intracellular form of vitamin B-12, cob(II)alamin. Superoxide is implicated in the pathophysiology of many inflammatory diseases, whereas vitamin B,2 derivatives are often beneficial in their treatment. We found that cob(II)alamin reacts with superoxide at rates approaching those of superoxide dismutase itself, suggesting a probable mechanism by which vitamin B-12. protects against chronic inflammation and modulates redox homeostasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1021/ja904670x" target="_blank" rel="noreferrer noopener">10.1021/ja904670x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2009
Binding
Birch C S
Brascht N E
chaperone
Chemistry
cobalamin
free-radicals
Journal Article
Journal of the American Chemical Society
McCaddon A
mechanism
nitric-oxide
oxidation
state
Suarez-Moreira E
Williams J H H
Yun J
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.redox.2014.10.004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.redox.2014.10.004</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
109-123
Volume
3
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Title
A name given to the resource
Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications
Publisher
An entity responsible for making the resource available
Redox Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014
Subject
The topic of the resource
Biochemistry & Molecular Biology; cell death; cytochrome-c-oxidase; hepatic ischemia-reperfusion; induced liver-injury; Mitochondrial dysfunction; Mitochondrial proteins; nadp(+)-dependent isocitrate dehydrogenase; nitric-oxide; Nitroxidative stress; oxidative stress; Post-translational modifications; rat-liver; Redox; synthase; targeted antioxidant mitoq; terminal kinase; Tissue injury
Creator
An entity primarily responsible for making the resource
Song B J; Akbar M; Abdelmegeed M A; Byun K; Lee B; Yoon S K; Hardwick J P
Description
An account of the resource
Mitochondria are critically important in providing cellular energy ATP as well as their involvement in anfi-oxiclant defense, fat oxidation, intermediary metabolism and cell death processes lt is well-established that mitochondrial functions are suppressed when living cells or organisms are exposed to potentially toxic agents including alcohol, high fat diets, smoking and certain drugs or in many pathophysiological states through increased levels of oxidative/nitrative stress. Under elevated nitroxidative stress, cellular macromolecules proteins, DNA, and lipids can undergo different oxidative modifications, leading to disruption of their normal, sometimes critical, physiological functions. Recent reports also indicated that many mitochondrial proteins are modified via various post-translation modifications (PTMs) and primarily inactivated. Because of the recently-emerging information, in this review, we specifically focus on the mechanisms and roles of five major PTMs (namely oxidation, nitration, phosphorylation, acetylation, and adduct formation with lipid-peroxides, reactive metabolites, or advanced glycation end products) in experimental models of alcoholic and nonalcoholic fatty liver disease as well as acute hepatic injury caused by toxic compounds. We also highlight the role of the ethanol-inducible cytochrome P450-2E1 (CYP2E1) in some of these PTM changes. Finally, we discuss translational research opportunities with natural and/or synthetic anti-oxidants, which can prevent or delay the onset of mitochondial dysfunction, fat accumulation and tissue injury. Published by Elsevier B.V.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.redox.2014.10.004" target="_blank" rel="noreferrer noopener">10.1016/j.redox.2014.10.004</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2014
Abdelmegeed M A
Akbar M
Biochemistry & Molecular Biology
Byun K
Cell Death
cytochrome-c-oxidase
Hardwick J P
hepatic ischemia-reperfusion
induced liver-injury
Journal Article
Lee B
Mitochondrial dysfunction
Mitochondrial proteins
nadp(+)-dependent isocitrate dehydrogenase
nitric-oxide
Nitroxidative stress
Oxidative Stress
Post-translational modifications
rat-liver
Redox
Redox Biology
Song B J
synthase
targeted antioxidant mitoq
terminal kinase
Tissue injury
Yoon S K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1155/2013/781050" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2013/781050</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
14-14
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Title
A name given to the resource
Increased Nitroxidative Stress Promotes Mitochondrial Dysfunction in Alcoholic and Nonalcoholic Fatty Liver Disease
Publisher
An entity responsible for making the resource available
Oxidative Medicine and Cellular Longevity
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013
Subject
The topic of the resource
aldehyde-dehydrogenase; ascorbate-dependent artifact; biotin-switch assay; Cell Biology; cytochrome-c-oxidase; hepatoma-cells; lipid-peroxidation; mediated oxidative stress; nitric-oxide; rat-liver; s-nitrosylation
Creator
An entity primarily responsible for making the resource
Song B J; Abdelmegeed M A; Henderson L E; Yoo S H; Wan J; Purohit V; Hardwick J P; Moon K H
Description
An account of the resource
Increased nitroxidative stress causes mitochondrial dysfunctions through oxidative modifications of mitochondrial DNA, lipids, and proteins. Persistent mitochondrial dysfunction sensitizes the target cells/organs to other pathological risk factors and thus ultimately contributes to the development of more severe disease states in alcoholic and nonalcoholic fatty liver disease. The incidences of nonalcoholic fatty liver disease continuously increase due to high prevalence of metabolic syndrome including hyperlipidemia, hypercholesterolemia, obesity, insulin resistance, and diabetes. Many mitochondrial proteins including the enzymes involved in fat oxidation and energy supply could be oxidatively modified (including S-nitrosylation/ nitration) under increased nitroxidative stress and thus inactivated, leading to increased fat accumulation and ATP depletion. To demonstrate the underlying mechanism(s) of mitochondrial dysfunction, we employed a redox proteomics approach using biotin-N-maleimide (biotin-NM) as a sensitive biotin-switch probe to identify oxidized Cys residues of mitochondrial proteins in the experimental models of alcoholic and acute liver disease. The aims of this paper are to briefly describe the mechanisms, functional consequences, and detection methods of mitochondrial dysfunction. We also describe advantages and limitations of the Cys-targeted redox proteomics method with alternative approaches. Finally, we discuss various applications of this method in studying oxidatively modified mitochondrial proteins in extrahepatic tissues or different subcellular organelles and translational research.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2013/781050" target="_blank" rel="noreferrer noopener">10.1155/2013/781050</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2013
Abdelmegeed M A
aldehyde-dehydrogenase
ascorbate-dependent artifact
biotin-switch assay
Cell Biology
cytochrome-c-oxidase
Hardwick J P
Henderson L E
hepatoma-cells
Journal Article
lipid-peroxidation
mediated oxidative stress
Moon K H
nitric-oxide
Oxidative Medicine and Cellular Longevity
Purohit V
rat-liver
s-nitrosylation
Song B J
Wan J
Yoo S H
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M212659200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M212659200</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
24461-24468
Issue
27
Volume
278
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Title
A name given to the resource
Angiotensin II enhances adenylyl cyclase signaling via Ca2+/calmodulin - G(q-)G(s) cross-talk regulates collagen production in cardiac fibroblasts
Publisher
An entity responsible for making the resource available
Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
2003-07
Subject
The topic of the resource
a(2b) receptors; adenosine inhibits collagen; Biochemistry & Molecular Biology; caveolae; Heart failure; in-vivo; nitric-oxide; pathway; protein-synthesis; smooth-muscle cells; ventricular myocytes
Creator
An entity primarily responsible for making the resource
Ostrom R S; Naugle J E; Hase M; Gregorian C; Swaney J S; Insel P A; Brunton L L; Meszaros J G
Description
An account of the resource
Cardiac fibroblasts regulate formation of extracellular matrix in the heart, playing key roles in cardiac remodeling and hypertrophy. In this study, we sought to characterize cross-talk between G(q) and G(s) signaling pathways and its impact on modulating collagen synthesis by cardiac fibroblasts. Angiotensin II (ANG II) activates cell proliferation and collagen synthesis but also potentiates cyclic AMP ( cAMP) production stimulated by beta-adrenergic receptors (beta-AR). The potentiation of beta-AR-stimulated cAMP production by ANG II is reduced by phospholipase C inhibition and enhanced by overexpression of G(q). Ionomycin and thapsigargin increased intracellular Ca2+ levels and potentiated isoproterenol- and forskolin-stimulated cAMP production, whereas chelation of Ca2+ with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid/AM inhibited such potentiation. Inhibitors of tyrosine kinases, protein kinase C, or Gbetagamma did not alter this cross-talk. Immunoblot analyses showed prominent expression of adenylyl cyclase 3 (AC3), a Ca2+-activated isoform, along with AC2, AC4, AC5, AC6, and AC7. Of those isoforms, only AC3 and AC5/6 proteins were detected in caveolin-rich fractions. Overexpression of AC6 increased betaAR-stimulated cAMP accumulation but did not alter the size of the ANG II potentiation, suggesting that the cross-talk is AC isoform-specific. Isoproterenol-mediated inhibition of serum-stimulated collagen synthesis increased from 31 to 48% in the presence of ANG II, indicating that betaAR-regulated collagen synthesis increased in the presence of ANG II. These data indicate that ANG II potentiates cAMP formation via Ca2+-dependent activation of AC activity, which in turn attenuates collagen synthesis and demonstrates one functional consequence of crosstalk between G(q) and G(s) signaling pathways in cardiac fibroblasts.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M212659200" target="_blank" rel="noreferrer noopener">10.1074/jbc.M212659200</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2003
a(2b) receptors
adenosine inhibits collagen
Biochemistry & Molecular Biology
Brunton L L
caveolae
Gregorian C
Hase M
Heart failure
in-vivo
Insel P A
Journal Article
Journal of Biological Chemistry
Meszaros J G
Naugle J E
nitric-oxide
Ostrom R S
pathway
protein-synthesis
smooth-muscle cells
Swaney J S
ventricular myocytes
-
Text
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<a href="http://doi.org/10.1186/1477-7827-6-64" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/1477-7827-6-64</a>
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10-10
Volume
6
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Title
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Delineation of VEGF-regulated genes and functions in the cervix of pregnant rodents by DNA microarray analysis
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Reproductive Biology and Endocrinology
Date
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2008
2008-12
Subject
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cells; Endocrinology & Metabolism; endothelial growth-factor; estrogen; factor expression; nitric-oxide; parturition; rat; Reproductive Biology; tissue; tumor angiogenesis; vascular-permeability
Creator
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Mowa C N; Li T B; Jesmin S; Folkesson H G; Usip S E; Papka R E; Hou G C
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Background: VEGF-regulated genes in the cervices of pregnant and non-pregnant rodents (rats and mice) were delineated by DNA microarray and Real Time PCR, after locally altering levels of or action of VEGF using VEGF agents, namely siRNA, VEGF receptor antagonist and mouse VEGF recombinant protein. Methods: Tissues were analyzed by genome-wide DNA microarray analysis, Real-time and gel-based PCR, and SEM, to decipher VEGF function during cervical remodeling. Data were analyzed by EASE score (microarray) and ANOVA (Real Time PCR) followed by Scheffe's F-test for multiple comparisons. Results: Of the 30,000 genes analyzed, about 4,200 genes were altered in expression by VEGF, i.e., expression of about 2,400 and 1,700 genes were down- and up-regulated, respectively. Based on EASE score, i.e., grouping of genes according to their biological process, cell component and molecular functions, a number of vascular- and non-vascular-related processes were found to be regulated by VEGF in the cervix, including immune response (including inflammatory), cell proliferation, protein kinase activity, and cell adhesion molecule activity. Of interest, mRNA levels of a select group of genes, known to or with potential to influence cervical remodeling were altered. For example, real time PCR analysis showed that levels of VCAM-1, a key molecule in leukocyte recruitment, endothelial adhesion, and subsequent trans-endothelial migration, were elevated about 10 folds by VEGF. Further, VEGF agents also altered mRNA levels of decorin, which is involved in cervical collagen fibrillogenesis, and expression of eNO, PLC and PKC mRNA, critical downstream mediators of VEGF. Of note, we show that VEGF may regulate cervical epithelial proliferation, as revealed by SEM. Conclusion: These data are important in that they shed new insights in VEGF's possible roles and mechanisms in cervical events near-term, including cervical remodeling.
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<a href="http://doi.org/10.1186/1477-7827-6-64" target="_blank" rel="noreferrer noopener">10.1186/1477-7827-6-64</a>
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Journal Article
2008
Cells
Endocrinology & Metabolism
endothelial growth-factor
estrogen
factor expression
Folkesson H G
Hou G C
Jesmin S
Journal Article
Li T B
Mowa C N
nitric-oxide
Papka R E
Parturition
rat
Reproductive Biology
Reproductive Biology and Endocrinology
tissue
tumor angiogenesis
Usip S E
vascular-permeability