LncRNA Fendrr inhibits hypoxia/reoxygenation-induced cardiomyocyte apoptosis by downregulating p53 expression.
Abstract
LncRNA Fendrr plays an important role in cardiac development, but its role in myocardial ischaemia-reperfusion (I/R) injury remains unclear. P53 has been shown to be an important regulator of apoptosis and is involved in myocardial I/R-induced apoptosis. This study aims at investigating whether Fendrr affects hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis through p53. The left anterior descending coronary artery of the rat was ligated for 30 min and then reperfusion for 120 min by releasing the suture. Neonatal rat ventricular myocytes (NRVM) and rat cardiac cell line H9c2 were cultured for 6 h in hypoxia (95% N2 and 5% CO2 ), followed by reoxygenation (95% air and 5% CO2 ) for 6 h. Transfection were performed in cells. Apoptosis was detected by flow cytometry. Moreover, RNA pull-down, RNA immunoprecipitation, ubiquitination assay, GST pull-down assay and co-immunoprecipitation were used to detect the regulation of Fendrr on p53 protein. Fendrr was decreased in I/R-induced myocardium and H/R-induced cardiomyocyte, and overexpression of Fendrr inhibited H/R-induced NRVM or H9c2 cells apoptosis. Further research found that the 1381-2100 nt of Fendrr bound to p53 protein and Fendrr promoted t direct binding of p53 to ...Continue Reading
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