Regulation of coronary collateral growth by microrna-21 in metabolic syndrome

Title

Regulation of coronary collateral growth by microrna-21 in metabolic syndrome

Creator

Juguilon C;Richardson D;Gadd J;Enrick M;Jamaiyar A;Xu Y;Wang Z;Wang T;Kolz C;Chilian W;Yin L

Publisher

Faseb Journal

Date

2020
2020-04

Description

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.

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).

Format

journalArticle

Search for Full-text

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Issue

1

Volume

34

ISSN

0892-6638

NEOMED College

NEOMED College of Medicine

NEOMED Department

NEOMED Postdoc Publications
NEOMED Student Publications
Department of Integrative Medical Sciences

Update Year & Number

September 2020 List

Citation

Juguilon C;Richardson D;Gadd J;Enrick M;Jamaiyar A;Xu Y;Wang Z;Wang T;Kolz C;Chilian W;Yin L, “Regulation of coronary collateral growth by microrna-21 in metabolic syndrome,” NEOMED Bibliography Database, accessed November 30, 2020, https://neomed.omeka.net/items/show/11307.

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