Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease

Epicardial fat is a continuously growing target of investigation in cardiovascular diseases due to both its anatomical proximity to the heart and coronary circulation and its unique physiology among adipose depots. Previous reports have demonstrated that epicardial fat plays key roles in coronary ar...

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Main Authors: Brendin Flinn, Christopher Adams, Nepal Chowdhury, Todd Gress, Nalini Santanam
Format: Article
Language:English
Published: MDPI AG 2022-05-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/10/5297
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author Brendin Flinn
Christopher Adams
Nepal Chowdhury
Todd Gress
Nalini Santanam
author_facet Brendin Flinn
Christopher Adams
Nepal Chowdhury
Todd Gress
Nalini Santanam
author_sort Brendin Flinn
collection DOAJ
description Epicardial fat is a continuously growing target of investigation in cardiovascular diseases due to both its anatomical proximity to the heart and coronary circulation and its unique physiology among adipose depots. Previous reports have demonstrated that epicardial fat plays key roles in coronary artery disease, but the non-coding RNA and transcriptomic alterations of epicardial fat in coronary artery disease have not been investigated thoroughly. Micro- and lncRNA microarrays followed by GO-KEGG functional enrichment analysis demonstrated sex-dependent unique mi/lncRNAs altered in human epicardial fat in comparison to subcutaneous fat in both patients with and without coronary artery disease (IRB approved). Among the 14 differentially expressed microRNAs in epicardial fat between patients with and without coronary artery disease, the hsa-miR-320 family was the most highly represented. IPW lncRNA interacted with three of these differentially expressed miRNAs. Next-generation sequencing and pathway enrichment analysis identified six unique mRNAs–miRNA pairs. Pathway enrichment identified inflammation, adipogenesis, and cardiomyocyte apoptosis as the most represented functions altered by the mi/lncRNAs and atherosclerosis and myocardial infarction among the highest cardiovascular pathologies associated with them. Overall, the epicardial fat in patients with coronary artery disease has a unique mi/lncRNA profile which is sex-dependent and has potential implications for regulating cardiac function.
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spelling doaj.art-0c288d1add04497cb6245f55d8fa7c962023-11-23T11:20:15ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-05-012310529710.3390/ijms23105297Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery DiseaseBrendin Flinn0Christopher Adams1Nepal Chowdhury2Todd Gress3Nalini Santanam4Department of Biomedical Sciences, Joan C Edwards School of Medicine, Marshall University, Huntington, WV 25755, USADepartment of Cardiology, Joan C Edwards School of Medicine, Marshall University, Huntington, WV 25755, USADepartment of Cardiovascular and Thoracic Surgery, St. Mary’s Medical Center, Huntington, WV 25702, USAResearch Service, Hershel “Woody” Williams VA Medical Center, Huntington, WV 25704, USADepartment of Biomedical Sciences, Joan C Edwards School of Medicine, Marshall University, Huntington, WV 25755, USAEpicardial fat is a continuously growing target of investigation in cardiovascular diseases due to both its anatomical proximity to the heart and coronary circulation and its unique physiology among adipose depots. Previous reports have demonstrated that epicardial fat plays key roles in coronary artery disease, but the non-coding RNA and transcriptomic alterations of epicardial fat in coronary artery disease have not been investigated thoroughly. Micro- and lncRNA microarrays followed by GO-KEGG functional enrichment analysis demonstrated sex-dependent unique mi/lncRNAs altered in human epicardial fat in comparison to subcutaneous fat in both patients with and without coronary artery disease (IRB approved). Among the 14 differentially expressed microRNAs in epicardial fat between patients with and without coronary artery disease, the hsa-miR-320 family was the most highly represented. IPW lncRNA interacted with three of these differentially expressed miRNAs. Next-generation sequencing and pathway enrichment analysis identified six unique mRNAs–miRNA pairs. Pathway enrichment identified inflammation, adipogenesis, and cardiomyocyte apoptosis as the most represented functions altered by the mi/lncRNAs and atherosclerosis and myocardial infarction among the highest cardiovascular pathologies associated with them. Overall, the epicardial fat in patients with coronary artery disease has a unique mi/lncRNA profile which is sex-dependent and has potential implications for regulating cardiac function.https://www.mdpi.com/1422-0067/23/10/5297epicardial adipose tissuenon-coding RNAscoronary artery diseasesex differences
spellingShingle Brendin Flinn
Christopher Adams
Nepal Chowdhury
Todd Gress
Nalini Santanam
Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease
International Journal of Molecular Sciences
epicardial adipose tissue
non-coding RNAs
coronary artery disease
sex differences
title Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease
title_full Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease
title_fullStr Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease
title_full_unstemmed Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease
title_short Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease
title_sort profiling of non coding regulators and their targets in epicardial fat from patients with coronary artery disease
topic epicardial adipose tissue
non-coding RNAs
coronary artery disease
sex differences
url https://www.mdpi.com/1422-0067/23/10/5297
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