1
40
7
-
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/10.1139/cjpp-2020-0581" target="_blank" rel="noreferrer noopener">http://doi.org/10.1139/cjpp-2020-0581</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).
ISSN
1205-7541 0008-4212
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1139/cjpp-2020-0581" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1139/cjpp-2020-0581</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
February 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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
Micro-RNA Regulation of Vascular Smooth Muscle Cells and Its Significance in Cardiovascular Diseases.
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-02-02
Subject
The topic of the resource
Cardiovascular Diseases; vascular; micro-RNA
Creator
An entity primarily responsible for making the resource
Nguyen DND;Chilian WM;Zain SM;Daud MF;Pung YF
Description
An account of the resource
Cardiovascular disease (CVD) is among the leading causes of death worldwide. Micro-RNAs (miRNAs), regulatory molecules that repress protein expression, have attracted considerable attention in CVD research. The vasculature plays a big role in CVD development and progression and dysregulation of vascular cells underlies the root of many vascular diseases. This review provides a brief introduction of the biogenesis of miRNAs and exosomes, followed by overview of the regulatory mechanisms of miRNAs in vascular smooth muscle cells (VSMCs) intracellular signaling during phenotypic switching, senescence, calcification and neointimal hyperplasia. Evidence of extracellular signaling of VSMCs and other cells via exosomal and circulating miRNAs was also presented. Lastly, current drawbacks and limitations of miRNA studies in CVD research and potential ways to overcome these disadvantages were discussed in detail. In-depth understanding of VSMC regulation via miRNAs will add substantial knowledge and advance research in diagnosis, disease progression and/or miRNA-derived therapeutic approaches in CVD research.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1139/cjpp-2020-0581" target="_blank" rel="noreferrer noopener">10.1139/cjpp-2020-0581</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
Publisher
An entity responsible for making the resource available
Canadian Journal Of Physiology And Pharmacology
2021
Canadian journal of physiology and pharmacology
CARDIOVASCULAR diseases
Chilian WM
Daud MF
Department of Integrative Medical Sciences
February 2021 List
journalArticle
micro-RNA
NEOMED College of Medicine
Nguyen DND
Pung YF
Vascular
Zain SM
-
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/10.1194/jlr.M039347" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M039347</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
2754-2762
Issue
10
Volume
54
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
Saturated Fatty Acids Activate Erk Signaling To Downregulate Hepatic Sortilin 1 In Obese And Diabetic Mice
Publisher
An entity responsible for making the resource available
Journal of Lipid Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-10
Subject
The topic of the resource
apolipoprotein-b secretion; Biochemistry & Molecular Biology; cells; diabetes; extracellular signal-regulated kinase; fatty liver; function; induced insulin-resistance; ldl; lipid metabolism; liver; mitogen-activated protein kinase; obesity; overproduction; oxidative stress; ubiquitination; vascular; vldl production
Creator
An entity primarily responsible for making the resource
Bi L P; Chiang J Y L; Ding W X; Dunn W; Roberts B; Li T G
Description
An account of the resource
Hepatic VLDL overproduction is a characteristic feature of diabetes and an important contributor to diabetic dyslipidemia. Hepatic sortilin 1 (Sort1), a cellular trafficking receptor, is a novel regulator of plasma lipid metabolism and reduces plasma cholesterol and triglycerides by inhibiting hepatic apolipoprotein B production. Elevated circulating free fatty acids play key roles in hepatic VLDL overproduction and the development of dyslipidemia. This study investigated the regulation of hepatic Sort1 in obesity and diabetes and the potential implications in diabetic dyslipidemia. Results showed that hepatic Sort1 protein was markedly decreased in mouse models of type I and type II diabetes and in human individuals with obesity and liver steatosis, whereas increasing hepatic Sort1 expression reduced plasma cholesterol and triglycerides in mice. Mechanistic studies showed that the saturated fatty acid palmitate activated extracellular signal-regulated kinase (ERK) and inhibited Sort1 protein by mechanisms involving Sort1 protein ubiquitination and degradation. Consistently, hepatic ERK signaling was activated in diabetic mice, whereas blocking ERK signaling by an ERK inhibitor increased hepatic Sort1 protein in mice. These results suggest that increased saturated fatty acids downregulate liver Sort1 protein, which may contribute to the development of dyslipidemia in obesity and diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M039347" target="_blank" rel="noreferrer noopener">10.1194/jlr.M039347</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
apolipoprotein-b secretion
Bi L P
Biochemistry & Molecular Biology
Cells
Chiang J Y L
Diabetes
Ding W X
Dunn W
extracellular signal-regulated kinase
Fatty Liver
Function
induced insulin-resistance
Journal Article or Conference Abstract Publication
Journal of lipid research
LDL
Li T G
Lipid Metabolism
Liver
mitogen-activated protein kinase
Obesity
overproduction
Oxidative Stress
Roberts B
ubiquitination
Vascular
vldl production
-
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
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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/10.1194/jlr.M039347" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M039347</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
2754-2762
Issue
10
Volume
54
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
Saturated Fatty Acids Activate Erk Signaling To Downregulate Hepatic Sortilin 1 In Obese And Diabetic Mice
Publisher
An entity responsible for making the resource available
Journal of Lipid Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-10
Subject
The topic of the resource
apolipoprotein-b secretion; Biochemistry & Molecular Biology; cells; diabetes; extracellular signal-regulated kinase; fatty liver; function; induced insulin-resistance; ldl; lipid metabolism; liver; mitogen-activated protein kinase; Obesity; overproduction; oxidative stress; ubiquitination; vascular; vldl production
Creator
An entity primarily responsible for making the resource
Bi L P; Chiang J Y L; Ding W X; Dunn W; Roberts B; Li T G
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M039347" target="_blank" rel="noreferrer noopener">10.1194/jlr.M039347</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
apolipoprotein-b secretion
Bi L P
Biochemistry & Molecular Biology
Cells
Chiang J Y L
Diabetes
Ding W X
Dunn W
extracellular signal-regulated kinase
Fatty Liver
Function
induced insulin-resistance
Journal of lipid research
LDL
Li T G
Lipid Metabolism
Liver
mitogen-activated protein kinase
Obesity
overproduction
Oxidative Stress
Roberts B
ubiquitination
Vascular
vldl production
-
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
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
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
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
22
Volume
128
Search for Full-text
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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
Lamin-Associated Protein 2a ( Lap2a) is a Novel Regulatory Switch for the Vascular Smooth Muscle Cell Contractile Gene Program
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
2013
2013-11
Subject
The topic of the resource
development; Cardiovascular System & Cardiology; Vascular; gene-expression; Myocardin; Smooth muscle regulation
Creator
An entity primarily responsible for making the resource
Carrao A C R; Chillian W C; Foisner R
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
2013
Cardiovascular System & Cardiology
Carrao A C R
Chillian W C
Circulation
development
Foisner R
gene-expression
Journal Article or Conference Abstract Publication
Myocardin
Smooth muscle regulation
Vascular
-
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
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
Endothelial Knockout of Polycystin 1 (PC1) Alters Mitochondrial Functions and Bioenergetics
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
Cardiovascular System & Cardiology; disease; Endothelial; Mitochondria; Reactive oxygen intermediates; Vascular
Creator
An entity primarily responsible for making the resource
Pung Y F; Adapala R K; Burke J R; Geldenhuys W J; Chilian W M; Thodeti C K; Jones T J
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
Adapala R K
Burke J R
Cardiovascular System & Cardiology
Chilian W M
Circulation
Disease
Endothelial
Geldenhuys W J
Jones T J
Journal Article
Mitochondria
Pung Y F
Reactive oxygen intermediates
Thodeti C K
Vascular