1
40
3
-
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/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/circ.142.suppl_3.17248</a>
Pages
A17248-A17248
Issue
Suppl 3
Volume
142
ISSN
0009-7322
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1161/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1161/circ.142.suppl_3.17248</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
December 2020 List
NEOMED College
NEOMED College of Medicine Student
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
NEOMED Student Publications
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
Abstract 17248: The role of microRNA-21 in regulating the coronary microcirculation in diabetes
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
2020
2020-11-17
Creator
An entity primarily responsible for making the resource
Juguilon C; Wang Z; Gadd J;Ohanyan VA; Anurag J; Molly E; Wang T; Kolz C; William MC; Yin L
Description
An account of the resource
Introduction: Coronary microvascular dysfunction is prevalent among diabetics and intersects with deficits in endothelial-dependent vasodilation. These deficits occur early in the progression of the disease, but the mechanisms remain incompletely understood. Nitric oxide (NO) is the major endothelial-dependent mediator of vasodilation in the healthy coronary circulation, but the mediator switches to hydrogen peroxide (H2O2) in coronary artery disease (CAD) patients. Diabetes is a risk factor for CAD, so we hypothesized that a similar switch would occur.Methods: Coronary arteries were isolated and endothelial-dependent vasodilation was assessed using myography. Quantitative polymerase chain reaction (qPCR) was performed for gene expression analysis and myocardial blood flow (MBF) was measured by contrast echocardiography.Results: Nitric oxide synthase inhibitor (L-NAME) inhibited vasodilation in wild type (WT) mice, but the H2O2 scavenger (PEG-catalase) had no effect. In contrast, vasodilation in diabetic mice was blunted by PEG-catalase, but not L-NAME. This suggests that the mediator of coronary vasodilation switched from NO to H2O2 in diabetes. Importantly, we found that microRNA-21 (miR-21) is upregulated in diabetes and the deficiency modulates the mediator switch from NO to H2O2 in diabetic mice.Conclusions: The switch in the mediator of coronary vasodilation from NO to H2O2 contributes to microvascular dysfunction in diabetes and miR-21 regulates this switch. Further genetic profiling will elucidate the pathways and mechanisms converging with miR-21 to regulate microvascular function in diabetes. This is the first mouse model that recapitulates the switch in mediator of coronary vasodilation from NO to H2O2 seen in CAD patients.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">10.1161/circ.142.suppl_3.17248</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
Anurag J
Circulation
December 2020 List
Department of Integrative Medical Sciences
Gadd J
journalArticle
Juguilon C
Kolz C
Molly E
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED Student Publications
Ohanyan VA
Wang T
Wang Z
William MC
Yin 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/10.1096/fasebj.2020.34.s1.09506" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fasebj.2020.34.s1.09506</a>
Issue
1
Volume
34
ISSN
0892-6638
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1096/fasebj.2020.34.s1.09506" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1096/fasebj.2020.34.s1.09506</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
September 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
NEOMED Postdoc Publications
NEOMED Student Publications
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
Regulation of coronary collateral growth by microrna-21 in metabolic syndrome
Publisher
An entity responsible for making the resource available
Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Creator
An entity primarily responsible for making the resource
Juguilon C;Richardson D;Gadd J;Enrick M;Jamaiyar A;Xu Y;Wang Z;Wang T;Kolz C;Chilian W;Yin L
Description
An account of the resource
Well‐developed coronary collaterals prove to be highly beneficial in salvaging ischemic myocardium, preserving cardiac function, and improving patient outcome post‐occlusion. However, this process of coronary collateral growth (CCG) is impaired in patients with metabolic syndrome. A complete understanding of the underlying mechanism, cell types, and genes contributing towards this impairment have yet to be elucidated. Therefore, uncovering more about the process may lead to potential therapeutics to induce CCG in metabolic syndrome. MicroRNA‐21 (miR‐21) is abundantly expressed in vascular and immune cells with numerous implications in cardiovascular disease including atherosclerosis, heart failure, and myocardial infarction. Furthermore, miR‐21 has been shown to regulate processes such as apoptosis, immune cell polarization, and endothelial progenitor proliferation. Additionally, miR‐21 dysregulation has been rooted in the diabetic population where lies a systemic inflammatory state. In this study, we investigated the role of miR‐21 in a mouse model of CCG. Our preliminary data suggested that down‐regulating miR‐21 rescues impaired CCG in a diet‐induced model of metabolic syndrome. Thus, we investigated the underlying mechanism and focused on the roles of miR‐21 in the maintenance of vascular homeostasis, function and inflammatory responses in metabolic syndrome. First, we studied whether miR‐21 regulates endothelial homeostasis by modulating the function and homing of bone marrow stem cells in metabolic syndrome. We analyzed endothelial progenitor cells (CD34+) in bone marrow and peripheral blood, along with endothelial proliferation in WT, miR‐21 knockout, and metabolic syndrome mice. Second, we studied whether miR‐21 regulates the inflammatory response in metabolic syndrome by characterizing bone marrow derived macrophages from WT and miR‐21 knockout animals along with mapping their influence on vascular cells. Third, we utilized a myeloid specific miR‐21 knockout to study its role during CCG in vivo. We found CCG to be blunted in these animals which suggests the importance of myeloid derived miR‐21 in healthy mice. Further studies will give us more insight on miR‐21 and its regulation of CCG in metabolic syndrome.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1096/fasebj.2020.34.s1.09506" target="_blank" rel="noreferrer noopener">10.1096/fasebj.2020.34.s1.09506</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
Chilian W
Department of Integrative Medical Sciences
Enrick M
Faseb Journal
Gadd J
Jamaiyar A
journalArticle
Juguilon C
Kolz C
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED College of Medicine Student
NEOMED Postdoc Publications
NEOMED Student Publications
Richardson D
September 2020 List
Wang T
Wang Z
Xu Y
Yin 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/10.1096/fasebj.2020.34.s1.09453" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fasebj.2020.34.s1.09453</a>
Issue
1
Volume
34
ISSN
0892-6638
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1096/fasebj.2020.34.s1.09453" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1096/fasebj.2020.34.s1.09453</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
September 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
NEOMED Postdoc Publications
NEOMED Student Publications
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
Sprouting angiogenesis contributes to coronary collateral growth induced by repetitive ischemia in adult mice
Publisher
An entity responsible for making the resource available
Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Creator
An entity primarily responsible for making the resource
Jamaiyar A;Juguilon C;Richardson D;Gadd J;Wang T;Enrick M;Goodner R;Chilian W;Yin L
Description
An account of the resource
In the United States, coronary heart diseases (CHD) are the leading cause of mortality and morbidity. A well‐developed coronary collateral circulation ameliorates the consequences of CHD, reducing the incidence of sudden death and infarct sizes following coronary occlusion. Stimulation of coronary collateral growth (CCG) is also an alternative therapeutic approach to patients with intractable angina pectoris. The importance of CCG is undisputable, but the process and mechanism underlying CCG is unclear. We developed a mouse model of CCG induced by repetitive ischemia (RI) and validated CCG by contrast echocardiography to measure the coronary blood flow in the normal zone (NZ) and the collateral dependent zone (CZ). We also used Micro‐CT scans to reconstruct the coronary vasculature in 3D and quantify CCG. In this study, we crossed ROSA mT/mG double fluorescent reporter mice with cell type‐specific cre mice to investigate the roles that different cell‐types play at various stages of CCG. Mice were subjected to the RI protocol and their cardiac function and coronary blood flow was measured by echocardiography. Following sacrifice, hearts were fixed for immunostaining or imaging under confocal and multiphoton microscopy. In ROSA mT/mG floxed, Apln cre mouse hearts, large vessels (diameter of 20–50 μm) expressing GFP were identified in the collateral dependent zone in the early stage of RI, indicating that they originated from sprouting endothelial cells. At the end of RI, a complete network of these vessels was observed anastomosing with existing vasculature from the NZ. Immunostaining revealed an outer layer of smooth muscle cells in these vessels, suggesting the arteriogenesis or arterialization. Interestingly, in ROSA mT/mG floxed, Lyz2 cre mouse hearts, GFP expressing myeloid cells were observed in high numbers around newly formed large vessels, suggesting that immune cell recruitment occurs in the early stages of CCG. Our preliminary data show that coronary collaterals form in response to RI, are of microvascular origin and are associated with early recruitment of immune cells to the CZ. Our further study will focus on the process of CCG in greater detail at the molecular and cellular level, potentially leading toward a therapeutic application of induced CCG in patients of ischemic heart diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1096/fasebj.2020.34.s1.09453" target="_blank" rel="noreferrer noopener">10.1096/fasebj.2020.34.s1.09453</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
Chilian W
Department of Integrative Medical Sciences
Enrick M
Faseb Journal
Gadd J
Goodner R
Jamaiyar A
journalArticle
Juguilon C
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED College of Medicine Student
NEOMED Postdoc Publications
NEOMED Student Publications
Richardson D
September 2020 List
Wang T
Yin L