CDKN2B-AS may indirectly regulate coronary artery disease-associated genes via targeting miR-92a

Ming Cheng1, Shoukuan An1, Junquan Li2

  • 1Department of Cardiac Surgery, The Second Affiliated Hospital of Harbin Medical University, Nangang, Harbin 150086, Heilongjiang, People's Republic of China.

Gene
|August 2, 2017
PubMed

Insights

This study investigated the pathogenesis of coronary artery disease (CAD) by analyzing gene expression data. Key genes like GATA2, MAP1B, and ARG1 were identified as potentially involved in CAD through a CDKN2B-AS-miR-92a regulatory network.

Area of Science:

  • Genomics and Bioinformatics
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Coronary artery disease (CAD) is a leading cause of mortality, encompassing conditions like angina, myocardial infarction, and sudden cardiac death.
  • Understanding the complex pathogenesis of CAD is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To explore the molecular mechanisms and pathogenesis underlying coronary artery disease (CAD).
  • To identify key genes, microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) involved in CAD development.

Main Methods:

  • Utilized gene expression datasets (GSE20680, GSE20681) from the Gene Expression Omnibus database.
  • Identified differentially expressed genes (DEGs) and constructed regulatory networks involving miRNAs and lncRNAs using bioinformatics databases and tools.
  • Employed a support vector machine (SVM) classifier to identify feature genes for CAD classification.

Main Results:

  • Identified 1208 differentially expressed genes (DEGs) and 5 CAD-associated miRNAs, including miR-92a.
  • Constructed a lncRNA-miRNA-DEG regulatory network, revealing CDKN2B-AS targeting miR-92a.
  • Highlighted GATA2, MAP1B, and ARG1 as key genes within the CDKN2B-AS-miR-92a regulatory network.

Conclusions:

  • The lncRNA CDKN2B-AS, through its regulation of miR-92a, potentially influences CAD pathogenesis.
  • GATA2, MAP1B, and ARG1 are implicated in CAD, possibly via indirect regulation by CDKN2B-AS and miR-92a.
Abstract

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