Long Non-coding RNA XIST Promotes the Proliferation of Cardiac Fibroblasts and the Accumulation of Extracellular Matrix by Sponging MicroRNA-155-5p

Overview

Journal Exp Ther Med

Specialty Pathology

Date 2021 Mar 26

PMID 33767772

Citations 10

Authors

Hongbin Zhang

Jianfei Ma

Fei Liu

Jun Zhang

Affiliations

Soon will be listed here.

Abstract

Acute myocardial infarction (AMI) is characterized by cardiomyocyte death followed by myocardial fibrosis, eventually leading to heart failure. Long non-coding (lnc)RNA X-inactive specific transcript (XIST) serves a vital role in the regulation of fibrosis. The aim of the present study was to determine whether myocardial fibrosis may be regulated by XIST and to elucidate the underlying mechanism. The relative mRNA expression levels of the target genes were evaluated using reverse transcription-quantitative polymerase chain reaction. Cell viability and apoptosis were determined using a Cell Counting Kit-8 assay and flow cytometry, respectively. The apoptosis and fibrosis-related protein expression levels were detected using western blot analysis. Finally, the interaction between XIST and microRNA (miR)-155-5p was analyzed using a luciferase reporter assay. XIST-overexpression increased proliferation and the expression level of the fibrosis-related proteins in the human cardiac fibroblast cells (HCFs). XIST directly targeted miR-155-5p and downregulated its expression, while miR-155-5p downregulation abolished the effect of XIST-silencing on cell viability and the expression level of the fibrosis-related proteins in the HCFs. XIST promoted cell proliferation and the expression level of fibrosis-related proteins by sponging miR-155-5p. Therefore, XIST may represent a novel effective target for AMI treatment.

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