Overexpression of long non-coding RNA ANRIL promotes post-ischaemic angiogenesis and improves cardiac functions by targeting Akt.

ABSTRACT: Angiogenesis is critical for re-establishing the blood supply to the surviving myocardium after myocardial infarction (MI). Long non-coding RNA ANRIL (lncRNA-ANRIL) has been reported to regulate endothelial functions in cardiovascular diseases. This study was to determine the role of lncRNA-ANRIL in Akt regulation and cardiac functions after MI. Human umbilical vein endothelial cells (HUVECs) were exposed to oxygen-glucose deprivation (OGD) to mimic in vivo ischaemia. The MI model in mice was induced by ligating left anterior descending coronary artery. OGD remarkably decreased lncRNA-ANRIL expression level, reduced the phosphorylated levels of Akt and eNOS proteins, and inhibited NO release and cell viability, which were duplicated by shRNA-mediated gene knockdown of lncRNA-ANRIL. Convers

SUBMITTER: Huang Q 

PROVIDER: S-EPMC7299705 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature