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LncRNA KCNQ1OT1 contributes to cardiomyocyte apoptosis by targeting FUS in heart failure.

Abstract：

:Long noncoding RNAs (lncRNAs) have recently been recognized as the important regulators in cardiac diseases. This study was aimed to investigate the role and molecular mechanism of lncRNA KCNQ1OT1 in regulating cardiomyocyte apoptosis in heart failure (HF). The mouse model of HF was induced by doxorubicin (ADR). Cell apoptosis was detected by Hoechst and TUNEL staining. Molecule expressions were determined by qRT-PCR and western blot. The interaction between KCNQ1OT1 and Fused in sarcoma (FUS) was assessed by RNA immunoprecipitation (RIP) and RNA pull-down assays. KCNQ1OT1 was up-regulated in the myocardial tissues of HF mice and the ADR-stimulated mouse myocardial cell line (HL-1). KCNQ1OT1 overexpression promoted apoptosis of ADR-stimulated HL-1 cells, while KCNQ1OT1 knockdown caused the opposite effect. The RIP and RNA pull-down results showed that KCNQ1OT1 - bound to FUS and negatively regulated its protein level. Knockdown of FUS inhibited apoptosis of ADR-stimulated HL-1 cells and reversed the effect of KCNQ1OT1 overexpression on cardiomyocyte apoptosis. In vivo experiment showed that KCNQ1OT1 ovexpression improved myocardial histopathological changes, reduced myocardial fibrosis areas, down-regulated FUS expression, and inhibited cell apoptosis of HF mice. In conclusion, KCNQ1OT1 facilitates cardiomyocyte apoptosis by - targeting FUS in ADR-induced HF.

journal_name

Exp Mol Pathol

journal_title

Experimental and molecular pathology

authors

Lai L,Xu Y,Kang L,Yang J,Zhu G

doi

10.1016/j.yexmp.2020.104480

subject

Has Abstract

pub_date

2020-08-01 00:00:00

pages

104480

eissn

0014-4800

issn

1096-0945

pii

S0014-4800(19)30685-9

journal_volume

115

pub_type

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