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40
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Text
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<a href="http://doi.org/10.1161/ATVBAHA.120.314962" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.120.314962</a>
Pages
ATVBAHA120314962
ISSN
1524-4636 1079-5642
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January 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
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TSP-1 (thrombospondin-1) deficiency protects APOE(-/-) mice against leptin-induced atherosclerosis.
Publisher
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Arteriosclerosis, Thrombosis, and Vascular Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-12-17
Subject
The topic of the resource
atherosclerosis; leptin; obesity; smooth muscle; thrombospondins
Creator
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Ganguly R; Khanal S; Mathias A; Gupta S; Lallo J; Sahu S; Ohanyan VA; Patel A; Storm K; Datta S; Raman P
Description
An account of the resource
OBJECTIVE: Hyperleptinemia, hallmark of obesity, is a putative pathophysiologic trigger for atherosclerosis. We previously reported a stimulatory effect of leptin on TSP-1 (thrombospondin-1) expression, a proatherogenic matricellular protein implicated in atherogenesis. However, a causal role of TSP-1 in leptin-driven atherosclerosis remains unknown. Approach and Results: Seventeen-weeks-old ApoE(-/-) and TSP-1(-/-)/ApoE(-/-) double knockout mice, on normocholesterolemic diet, were treated with or without murine recombinant leptin (5 µg/g bwt, IP) once daily for 3 weeks. Using aortic root morphometry and en face lesion assay, we found that TSP-1 deletion abrogated leptin-stimulated lipid-filled lesion burden, plaque area, and collagen accumulation in aortic roots of ApoE(-/-) mice, shown via Oil red O, hematoxylin and eosin, and Masson trichrome staining, respectively. Immunofluorescence microscopy of aortic roots showed that TSP-1 deficiency blocked leptin-induced inflammatory and smooth muscle cell abundance as well as cellular proliferation in ApoE(-/-) mice. Moreover, these effects were concomitant to changes in VLDL (very low-density lipoprotein)-triglyceride and HDL (high-density lipoprotein)-cholesterol levels. Immunoblotting further revealed reduced vimentin and pCREB accompanied with augmented smooth muscle-myosin heavy chain expression in aortic vessels of leptin-treated double knockout versus leptin-treated ApoE(-/-); also confirmed in aortic smooth muscle cells from the mice genotypes, incubated ± leptin in vitro. Finally, TSP-1 deletion impeded plaque burden in leptin-treated ApoE(-/-) on western diet, independent of plasma lipid alterations. CONCLUSIONS: The present study provides evidence for a protective effect of TSP-1 deletion on leptin-stimulated atherogenesis. Our findings suggest a regulatory role of TSP-1 on leptin-induced vascular smooth muscle cell phenotypic transition and inflammatory lesion invasion. Collectively, these results underscore TSP-1 as a potential target of leptin-induced vasculopathy.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.120.314962" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.120.314962</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).
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journalArticle
2020
and vascular biology
Arteriosclerosis
Arteriosclerosis, thrombosis, and vascular biology
Atherosclerosis
Datta S
Department of Integrative Medical Sciences
Ganguly R
Gupta S
January 2021 List
journalArticle
Khanal S
Lallo J
leptin
Mathias A
NEOMED College of Medicine
Obesity
Ohanyan VA
Patel A
Raman P
Sahu S
smooth muscle
Storm K
Thrombosis
thrombospondins
-
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.
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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
2-2
Issue
22
Volume
128
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Dublin Core
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Title
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The Role of Vascular Smooth Muscle Kv 1.5 Channels in Coronary Metabolic Dilation
Publisher
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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
Blood; Cardiovascular System & Cardiology; Coronary circulation; flow; Heart failure; Ion channels; Smooth muscle
Creator
An entity primarily responsible for making the resource
Ohanyan V A; Luli J; Yin L Y; Logan S; Enrick M; Stevanov K; Kolz C L; Kmetz J; Bratz I; Chilian W M
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n/a
Format
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Journal Article
2013
Blood
Bratz I
Cardiovascular System & Cardiology
Chilian W M
Circulation
Coronary Circulation
Enrick M
flow
Heart failure
Ion Channels
Journal Article
Kmetz J
Kolz C L
Logan S
Luli J
Ohanyan V A
smooth muscle
Stevanov K
Yin L Y
-
Text
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URL Address
<a href="http://doi.org/10.3390/ijms22115446" target="_blank" rel="noreferrer noopener">http://doi.org/10.3390/ijms22115446</a>
Issue
11
Volume
22
ISSN
1422-0067
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.3390/ijms22115446" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.3390/ijms22115446</a>
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Update Year & Number
June 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
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Leptin in Atherosclerosis: Focus on Macrophages, Endothelial and Smooth Muscle Cells.
Publisher
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International Journal Of Molecular Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-05-21
Subject
The topic of the resource
Humans; atherosclerosis; Animals; endothelial cells; macrophages; vascular smooth muscle cells; Leptin/metabolism; Atherosclerosis/metabolism; Diabetes Mellitus/metabolism; Endothelial Cells/metabolism; hyperleptinemia; Macrophages/metabolism; Myocytes Smooth Muscle/metabolism; Obesity/metabolism; ADIPOSE tissue physiology; LEPTIN; LEPTIN receptors; MACROPHAGES; MUSCLE cells; SMOOTH muscle
Creator
An entity primarily responsible for making the resource
Raman P; Khanal S
Description
An account of the resource
Increasing adipose tissue mass in obesity directly correlates with elevated circulating leptin levels. Leptin is an adipokine known to play a role in numerous biological processes including regulation of energy homeostasis, inflammation, vascular function and angiogenesis. While physiological concentrations of leptin may exhibit multiple beneficial effects, chronically elevated pathophysiological levels or hyperleptinemia, characteristic of obesity and diabetes, is a major risk factor for development of atherosclerosis. Hyperleptinemia results in a state of selective leptin resistance such that while beneficial metabolic effects of leptin are dampened, deleterious vascular effects of leptin are conserved attributing to vascular dysfunction. Leptin exerts potent proatherogenic effects on multiple vascular cell types including macrophages, endothelial cells and smooth muscle cells; these effects are mediated via an interaction of leptin with the long form of leptin receptor, abundantly expressed in atherosclerotic plaques. This review provides a summary of recent in vivo and in vitro studies that highlight a role of leptin in the pathogenesis of atherosclerotic complications associated with obesity and diabetes.
Identifier
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<a href="http://doi.org/10.3390/ijms22115446" target="_blank" rel="noreferrer noopener">10.3390/ijms22115446</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).
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journalArticle
2021
ADIPOSE tissue physiology
Animals
Atherosclerosis
Atherosclerosis/metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus/metabolism
endothelial cells
Endothelial Cells/metabolism
Humans
hyperleptinemia
International journal of molecular sciences
journalArticle
June 2021 List
Khanal S
leptin
LEPTIN receptors
Leptin/metabolism
Macrophages
Macrophages/metabolism
MUSCLE cells
Myocytes Smooth Muscle/metabolism
NEOMED College of Medicine
Obesity/metabolism
Raman P
smooth muscle
vascular 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.
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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
Volume
37
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
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Role of Thrombospondin-1 in Atherosclerotic Complications Associated With Metabolic Syndrome
Publisher
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Arteriosclerosis Thrombosis and Vascular Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-05
Subject
The topic of the resource
Atherosclerosis; Cardiovascular System & Cardiology; Hematology; Metabolic syndrome; Smooth muscle
Creator
An entity primarily responsible for making the resource
Sahu S; Ganguly R; Rea B; Cerroni A; Mathias A; Raman P
Identifier
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n/a
Format
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Journal Article
2017
Arteriosclerosis Thrombosis and Vascular Biology
Atherosclerosis
Cardiovascular System & Cardiology
Cerroni A
Ganguly R
Hematology
Journal Article
Mathias A
Metabolic syndrome
Raman P
Rea B
Sahu S
smooth muscle