1
40
9
-
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.00282.2010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00282.2010</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
H1938-H1949
Issue
5
Volume
300
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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
Angiotensin Type I Receptor Blockade In Conjunction With Enhanced Akt Activation Restores Coronary Collateral Growth In The 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
2011
2011-05
Subject
The topic of the resource
Cardiovascular System & Cardiology; coronary artery occlusion; endothelial-cells; inhibition; ischemia-induced angiogenesis; kinase; mediated angiogenesis; nitric-oxide synthase; pathway; phosphorylation; Physiology; rat; smooth-muscle-cells; transient
Creator
An entity primarily responsible for making the resource
Jadhav R; Dodd T; Smith E; Bailey E; DeLucia A L; Russell J C; Madison R; Potter B; Walsh K; Jo H J; Rocic P
Description
An account of the resource
Jadhav R, Dodd T, Smith E, Bailey E, DeLucia AL, Russell JC, Madison R, Potter B, Walsh K, Jo H, Rocic P. Angiotensin type I receptor blockade in conjunction with enhanced Akt activation restores coronary collateral growth in the metabolic syndrome. Am J Physiol Heart Circ Physiol 300: H1938-H1949, 2011. First published February 18, 2011; doi:10.1152/ajpheart.00282.2010.-We have previously demonstrated that Akt was required for repetitive ischemia (RI)-induced coronary collateral growth (CCG) in healthy rats but was not activated by RI in the metabolic syndrome (JCR:LA-cp rats) where CCG was impaired. Here we hypothesized that failure of angiotensin type I receptor (AT(1)R) blockers to restore Akt activation is a key determinant of their inability to completely restore CCG in the metabolic syndrome. Therefore, we investigated whether adenovirus-mediated delivery of constitutively active Akt (MyrAkt-Adv.) in conjunction with AT(1)R blockade (candesartan) was able to restore RI-induced CCG in JCR:LA-cp rats. Successful myocardial MyrAkt-Adv delivery was confirmed by a >80% transduction efficiency and an approximately fourfold increase in Akt expression and activation. CCG was assessed by myocardial blood flow measurements in the normal and collateral-dependent zones. MyrAkt-Adv alone significantly increased RI-induced CCG in JCR:LA-cp rats (similar to 30%), but it completely restored CCG in conjunction with administration of candesartan. In contrast, dominant negative Akt (DN-Akt-Adv) reversed the beneficial effect of candesartan on CCG in JCR:LA-cp rats. We conclude that optimal restoration of coronary collateral growth in JCR:LA-cp rats requires a combination of AT(1)R blockade with constitutive Akt activation. These findings may carry implications for metabolic syndrome patients in need of coronary revascularization.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00282.2010" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00282.2010</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
American Journal of Physiology-Heart and Circulatory Physiology
Bailey E
Cardiovascular System & Cardiology
coronary artery occlusion
DeLucia A L
Dodd T
endothelial-cells
inhibition
ischemia-induced angiogenesis
Jadhav R
Jo H J
Journal Article or Conference Abstract Publication
Kinase
Madison R
mediated angiogenesis
nitric-oxide synthase
pathway
Phosphorylation
Physiology
Potter B
rat
Rocic P
Russell J C
Smith E
smooth-muscle-cells
transient
Walsh 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/10.1210/en.2004-0728" target="_blank" rel="noreferrer noopener">http://doi.org/10.1210/en.2004-0728</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
5157-5167
Issue
11
Volume
145
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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
Differential Regulation Of The Cell Cycle By Alpha(1)-adrenergic Receptor Subtypes
Publisher
An entity responsible for making the resource available
Endocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
2004-11
Subject
The topic of the resource
adventitial fibroblasts; alpha(1b)-adrenergic receptor; arterial blood-pressure; dna-synthesis; Endocrinology & Metabolism; fibroblasts; gene-expression; kinase pathways; mitogen-activated protein; proliferation; rat-1; smooth-muscle-cells
Creator
An entity primarily responsible for making the resource
Gonzalez-Cabrera P J; Shi T; Yun J; McCune D F; Rorabaugh B R; Perez D M
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1210/en.2004-0728" target="_blank" rel="noreferrer noopener">10.1210/en.2004-0728</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2004
adventitial fibroblasts
alpha(1b)-adrenergic receptor
arterial blood-pressure
dna-synthesis
Endocrinology
Endocrinology & Metabolism
fibroblasts
gene-expression
Gonzalez-Cabrera P J
kinase pathways
McCune D F
mitogen-activated protein
Perez D M
proliferation
rat-1
Rorabaugh B R
Shi T
smooth-muscle-cells
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
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
H1720-H1727
Issue
4
Volume
281
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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
Testosterone relaxes coronary arteries by opening the large-conductance, calcium-activated potassium channel
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
2001
2001-10
Subject
The topic of the resource
rat; vasodilation; ion channel; Physiology; Cardiovascular System & Cardiology; disease; smooth-muscle-cells; aorta; men; Vascular; hormones; androgen; steroid
Creator
An entity primarily responsible for making the resource
Deenadayalu V U P; White R E; Stallone J N; Gao X M; Garcia A J
Description
An account of the resource
Cardiovascular diseases are often considered to be a predominantly male health problem, and it has been suggested that testosterone exerts deleterious effects on cardiovascular function; however, few experimental studies support this suggestion. Moreover, the cellular and molecular mechanism(s) underlying vascular responses to testosterone is unknown. The present study has investigated the acute effects of testosterone on porcine coronary artery smooth muscle at the tissue and cellular levels. Contractile studies demonstrated that testosterone or dihydrotestosterone (a nonaromatizable metabolite) relaxed these arteries by an endothelium-independent mechanism involving potassium efflux. Direct evidence from patch-clamp studies confirmed that testosterone opened K+ channels in single coronary myocytes, and further analysis identified this protein as the large-conductance, calcium- and voltage-activated potassium (BKCa) channel. Moreover, inhibiting BKCa channel activity significantly attenuated testosterone-induced coronary relaxation. These findings indicate that testosterone relaxes porcine coronary arteries predominantly by opening BKCa channels in coronary myocytes, and this response may be associated with accumulation of cGMP. This novel mechanism may provide a better understanding of testosterone-induced vasorelaxation reported in recent experimental and early clinical studies.
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
2001
American Journal of Physiology-Heart and Circulatory Physiology
androgen
Aorta
Cardiovascular System & Cardiology
Deenadayalu V U P
Disease
Gao X M
Garcia A J
Hormones
ion channel
Journal Article or Conference Abstract Publication
men
Physiology
rat
smooth-muscle-cells
Stallone J N
Steroid
Vascular
vasodilation
White R E
-
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.bbabio.2011.03.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbabio.2011.03.001</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
491-502
Issue
5
Volume
1807
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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
Excess no predisposes mitochondrial succinate-cytochrome c reductase to produce hydroxyl radical
Publisher
An entity responsible for making the resource available
Biochimica Et Biophysica Acta-Bioenergetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-05
Subject
The topic of the resource
Mitochondria; Biophysics; oxygen; Biochemistry & Molecular Biology; nitric-oxide synthase; reactive; smooth-muscle-cells; endothelial-cells; reperfusion injury; EPR; postischemic heart; complex-ii; Electron transport chain; electron-transport; Hydroxyl radical; NO; oxygen-free radicals; SCR; spin trapping; superoxide generation
Creator
An entity primarily responsible for making the resource
Chen J F; Chen C L; Alevriadou B R; Zweier J L; Chen Y R
Description
An account of the resource
Mitochondria-derived oxygen-free radical(s) are important mediators of oxidative cellular injury. It is widely hypothesized that excess NO enhances O(2)(center dot-) generated by mitochondria under certain pathological conditions. In the mitochondrial electron transport chain, succinate-cytochrome c reductase (SCR) catalyzes the electron transfer reaction from succinate to cytochrome c. To gain the insights into the molecular mechanism of how NO overproduction may mediate the oxygen-free radical generation by SCR, we employed isolated SCR, cardiac myoblast H9c2, and endothelial cells to study the interaction of NO with SCR in vitro and ex vivo. Under the conditions of enzyme turnover in the presence of NO donor (DEANO), SCR gained pro-oxidant function for generating hydroxyl radical as detected by EPR spin trapping using DEPMPO. The EPR signal associated with DEPMPO/(center dot)OH adduct was nearly completely abolished in the presence of catalase or an iron chelator and partially inhibited by SOD, suggesting the involvement of the iron-H(2)O(2)-dependent Fenton reaction or O(2)(center dot-)-dependent Haber-Weiss mechanism. Direct EPR measurement of SCR at 77 K indicated the formation of a nonheme iron-NO complex, implying that electron leakage to molecular oxygen was enhanced at the FAD cofactor, and that excess NO predisposed SCR to produce (center dot)OH. In H9c2 cells, SCR-dependent oxygen-free radical generation was stimulated by NO released from DEANO or produced by the cells following exposure to hypoxia/reoxygenation. With shear exposure that led to overproduction of NO by the endothelium, SCR-mediated oxygen-free radical production was also detected in cultured vascular endothelial cells. (C) 2011 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.bbabio.2011.03.001" target="_blank" rel="noreferrer noopener">10.1016/j.bbabio.2011.03.001</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
Alevriadou B R
Biochemistry & Molecular Biology
Biochimica Et Biophysica Acta-Bioenergetics
Biophysics
Chen C L
Chen J F
Chen Y R
complex-ii
Electron transport chain
electron-transport
endothelial-cells
EPR
Hydroxyl radical
Journal Article or Conference Abstract Publication
Mitochondria
nitric-oxide synthase
NO
Oxygen
oxygen-free radicals
postischemic heart
reactive
Reperfusion Injury
SCR
smooth-muscle-cells
spin trapping
superoxide generation
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
<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
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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/10.1152/ajpheart.00888.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00888.2009</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
H1182-H1189
Issue
4
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
Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation
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
2010-04
Subject
The topic of the resource
potassium channels; exercise; Physiology; Cardiovascular System & Cardiology; blood flow; activation; smooth-muscle-cells; heart; adenosine; adenosine triphosphate-dependent; arterioles; calcium-activated potassium channels; cardiovascular-disease mortality; coronary reactive hyperemia; myocardial reactive hyperemia; Ossabaw miniature swine; sensitive potassium channels; type 2 diabetes; voltage-activated potassium channels
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Payne G A; Berwick Z 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, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol 298: H1182-H1189, 2010. First published January 29, 2010; doi: 10.1152/ajpheart.00888.2009.-This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K+ channels to coronary reactive hyperemia. Ca2+-activated (BKCa), voltage-activated (K-V), and ATP-dependent (K-ATP) K+ channels were investigated. Studies were conducted in anesthetized miniature 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) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BKCa (penitrem A; 10 mu g/kg iv), K-V (4-aminopyridine; 0.3 mg/kg iv) and K-ATP (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced similar to 30% compared with lean swine. Inhibition of BKCa channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of KV channels significantly reduced the repayment of flow debt (similar to 25%) in both lean and metabolic syndrome swine. Additional blockade of K-ATP channels further diminished (similar to 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K+ channels to reactive hyperemia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00888.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00888.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
activation
adenosine
adenosine triphosphate-dependent
Alloosh M
American Journal of Physiology-Heart and Circulatory Physiology
Arterioles
Berwick Z C
blood flow
Borbouse L
Bratz I N
calcium-activated potassium channels
Cardiovascular System & Cardiology
cardiovascular-disease mortality
coronary reactive hyperemia
Dick G M
Exercise
heart
Journal Article or Conference Abstract Publication
myocardial reactive hyperemia
Neeb Z P
Ossabaw miniature swine
Payne G A
Physiology
Potassium Channels
sensitive potassium channels
smooth-muscle-cells
Sturek M
Tune J D
Type 2 diabetes
voltage-activated potassium channels
-
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.00466.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00466.2009</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
H1629-H1637
Issue
5
Volume
297
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
Impaired function of coronary BKCa channels in 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
2009
2009-11
Subject
The topic of the resource
obesity; Physiology; Cardiovascular System & Cardiology; channels; smooth-muscle-cells; circulation; cardiovascular-disease; Ion channels; beta-1 subunit; activated potassium; arteriolar dilation; blood flow; ca2+-activated k+ channels; currents; diabetic fatty rats; induced relaxation; large-conductance; outward
Creator
An entity primarily responsible for making the resource
Borbouse L; Dick G M; Asano S; Bender S B; Dincer U D; Payne G A; Neeb Z P; Bratz I N; Sturek M; Tune J D
Description
An account of the resource
Borbouse L, Dick GM, Asano S, Bender SB, Dincer UD, Payne GA, Neeb ZP, Bratz IN, Sturek M, Tune JD. Impaired function of coronary BKCa channels in metabolic syndrome. Am J Physiol Heart Circ Physiol 297: H1629-H1637, 2009. First published September 11, 2009; doi:10.1152/ajpheart.00466.2009.-The role of large-conductance Ca2+-activated K+ (BKCa) channels in regulation of coronary microvascular function is widely appreciated, but molecular and functional changes underlying the deleterious influence of metabolic syndrome (MetS) have not been determined. Male Ossabaw miniature swine consumed for 3-6 mo a normal diet (11% kcal from fat) or an excess-calorie atherogenic diet that induces MetS (45% kcal from fat, 2% cholesterol, 20% kcal from fructose). MetS significantly impaired coronary vasodilation to the BKCa opener NS-1619 in vivo (30-100 mu g) and reduced the contribution of these channels to adenosine-induced microvascular vasodilation in vitro (1-100 mu M). MetS reduced whole cell penitrem A (1 mu M)-sensitive K+ current and NS-1619-activated (10 mu M) current in isolated coronary vascular smooth muscle cells. MetS increased the concentration of free intracellular Ca2+ and augmented coronary vasoconstriction to the L-type Ca2+ channel agonist BAY K 8644 (10 pM-10 nM). BKCa channel alpha and beta(1) protein expression was increased in coronary arteries from MetS swine. Coronary vascular dysfunction in MetS is related to impaired BKCa channel function and is accompanied by significant increases in L-type Ca2+ channel-mediated coronary vasoconstriction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00466.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00466.2009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
activated potassium
American Journal of Physiology-Heart and Circulatory Physiology
arteriolar dilation
Asano S
Bender S B
beta-1 subunit
blood flow
Borbouse L
Bratz I N
ca2+-activated k+ channels
Cardiovascular System & Cardiology
cardiovascular-disease
channels
Circulation
currents
diabetic fatty rats
Dick G M
Dincer U D
induced relaxation
Ion Channels
Journal Article or Conference Abstract Publication
large-conductance
Neeb Z P
Obesity
outward
Payne G A
Physiology
smooth-muscle-cells
Sturek M
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/10.1161/atvbaha.109.186189" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/atvbaha.109.186189</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
802-U56
Issue
6
Volume
29
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
Amplification of Coronary Arteriogenic Capacity of Multipotent Stromal Cells by Epidermal Growth Factor
Publisher
An entity responsible for making the resource available
Arteriosclerosis Thrombosis and Vascular Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-06
Subject
The topic of the resource
coronary circulation; angiogenesis; collateral circulation; Cardiovascular System & Cardiology; Myocardial infarction; expression; binding; Hematology; mesenchymal stem-cells; smooth-muscle-cells; rat model; endothelial-cells; collateral growth; improve heart function
Creator
An entity primarily responsible for making the resource
Belmadani S; Matrougui K; Kolz C; Pung Y F; Palen D; Prockop D J; Chilian W M
Description
An account of the resource
Objective-We determined whether increasing adherence of multipotent stromal cells (MSCs) would amplify their effects on coronary collateral growth (CCG). Methods and Results-Adhesion was established in cultured coronary endothelials cells (CECs) or MSCs treated with epidermal growth factor (EGF). EGF increased MSCs adhesion to CECs, and increased intercellular adhesion molecule (ICAM-1) or vascular cell adhesion molecule (VCAM-1) expression. Increased adherence was blocked by EGF receptor antagonism or antibodies to the adhesion molecules. To determine whether adherent MSCs, treated with EGF, would augment CCG, repetitive episodes of myocardial ischemia (RI) were introduced and CCG was measured from the ratio of collateral-dependent (CZ) and normal zone (NZ) flows. CZ/NZ was increased by MSCs without treatment versus RI-control and was further increased by EGF-treated MSCs. EGF-treated MSCs significantly improved myocardial function versus RI or RI + MSCs demonstrating that the increase in collateral flow was functionally significant. Engraftment of MSCs into myocardium was also increased by EGF treatment. Conclusions-These results reveal the importance of EGF in MSCs adhesion to endothelium and suggest that MSCs may be effective therapies for the stimulation of coronary collateral growth when interventions are used to increase their adhesion and homing (in vitro EGF treatment) to the jeopardized myocardium. (Arterioscler Thromb Vasc Biol. 2009; 29: 802-808.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/atvbaha.109.186189" target="_blank" rel="noreferrer noopener">10.1161/atvbaha.109.186189</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
angiogenesis
Arteriosclerosis Thrombosis and Vascular Biology
Belmadani S
Binding
Cardiovascular System & Cardiology
Chilian W M
Collateral Circulation
collateral growth
Coronary Circulation
endothelial-cells
expression
Hematology
improve heart function
Journal Article or Conference Abstract Publication
Kolz C
Matrougui K
mesenchymal stem-cells
myocardial infarction
Palen D
Prockop D J
Pung Y F
rat model
smooth-muscle-cells
-
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/10.5551/jat.29421" target="_blank" rel="noreferrer noopener">http://doi.org/10.5551/jat.29421</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
1317-1337
Issue
12
Volume
22
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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
Interleukin-1 Receptor-Associated Kinase 1/4 as a Novel Target for Inhibiting Neointimal Formation After Carotid Balloon Injury
Publisher
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Journal of Atherosclerosis and Thrombosis
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015
Subject
The topic of the resource
Cardiovascular System & Cardiology; in-vivo; smooth-muscle-cells; signaling pathways; hyperplasia; NF kappa B; arterial injury; bacterial infections; Carotid artery balloon injury; intimal; irak-4 protein; IRAK1/4; muscle cell; Neointimal formation; NF kappa B; TLR4; toll-like-receptor; toll-like-receptor-4 expression; Vascular smooth
Creator
An entity primarily responsible for making the resource
Bai S R; Li D Y; Zhou Z M; Cao J L; Xu T D; Zhang X T; Wang Y; Guo J S; Zhang Y B
Description
An account of the resource
Aim: Interleukin-1 receptor-associated kinase 1 (IRAK1) and IRAK4 play essential roles in the induction of inflammatory gene products. We aimed to investigate the effect of the inhibition of IRAK1 and IRAK4 kinase activities on neointimal formation in rats with carotid artery balloon injuries using the IRAK1/4 inhibitor N-(2-Morpholinylethyl)-2-(3-nitrobenzoylamido)-benzimidazole, a cell-permeable benzimidazole compound. Methods: Wistar rats and vascular smooth muscle cells (VSMCs) isolated from the thoracic aortas were used. Toll-like receptor 4 (TLR4)-mediated nuclear factor kappa B (NF kappa B) signaling pathway was revealed by microarrays analysis. In addition, the differential expression of the TLR4 pathway genes, including TLR4, IRAK1, I kappa B alpha, and interleukin-1 beta (IL-1 beta), was confirmed by quantitative real-time polymerase chain reaction. Immunohistochemical staining, elastic-van Gieson and Masson staining, 5-ethynyl-2'-deoxyuridine staining, enzyme-linked immunosorbent assay, transwell migration assay and western blotting were also contributed for relevant detection. Results: The expression of TLR4 protein gradually increased at days 1, 3, 7, and 21 after balloon injury compared with the uninjured group. The dual inhibition of IRAK1 and IRAK4 attenuated neointimal formation and fibrotic remodeling after injury in vivo and suppressed VSMC proliferation and migration in vitro. The production of mediators such as tumor necrosis factor-alpha and IL-1 beta in injured arteries were also reduced by the inhibition of IRAK1 and IRAK4. The expression of NF kappa B p65- and F4/80-positive cells in inhibitor rats were fewer than those in control rats at day 7, while IRAK1 expression was markedly higher at day 3 in inhibitor rats. Furthermore, western blotting analysis revealed that the IRAK1/4 inhibitor suppressed the IRAK1 and IRAK4 kinase activities and the activation of the TLR4-mediated NF kappa B pathway in vivo and in vitro. Conclusions: This study suggested that IRAK1/4 could serve as a potential therapeutic target to suppress neointimal formation in carotid arteries after balloon injury through the TLR4/NF kappa B signaling pathway.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.5551/jat.29421" target="_blank" rel="noreferrer noopener">10.5551/jat.29421</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2015
arterial injury
Bacterial Infections
Bai S R
Cao J L
Cardiovascular System & Cardiology
Carotid artery balloon injury
Guo J S
Hyperplasia
in-vivo
intimal
irak-4 protein
IRAK1/4
Journal Article or Conference Abstract Publication
Journal of Atherosclerosis and Thrombosis
Li D Y
muscle cell
Neointimal formation
NF kappa B
signaling pathways
smooth-muscle-cells
TLR4
toll-like-receptor
toll-like-receptor-4 expression
Vascular smooth
Wang Y
Xu T D
Zhang X T
Zhang Y B
Zhou Z M