Long non-coding RNA MALAT1 enhances the apoptosis of cardiomyocytes through autophagy inhibition by regulating TSC2-mTOR signaling

摘要

MALAT1 overexpression inhibited, whereas MALAT1 knockdown enhanced the autophagy of cardiomyocytes stimulated with H/R injury. Cardiomyocytes were isolated from neonatal mice and then stimulated with H/R injury. qRT-PCR analysis of relative MALAT1 level ( and HIF-1α mRNA level ( in cardiomyocytes. Western blot analysis of HIF-1α protein level in cardiomyocytes. LDH release in cardiomyocytes. The autophagosome puncta of GFP-LC3 by immunofluorescence in cardiomyocytes. Scale bar: 20 μm. Western blot was performed to examine the protein levels of LC3-I, LC3-II, and Beclin-1 in cardiomyocytes. Western blot was performed to examine the protein levels of LC3-I, LC3-II, and Beclin-1 in cardiomyocytes which were transfected with pcDNA3.1-MALAT1 (MALAT1), empty pcDNA3.1 (Vector), si-MALAT1, or scramble siRNA (si-Ctrl), followed by stimulation with H/R injury. Their quantitative analysis was normalized to β-actin. – **p g **p ##p