Fig. 1.

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 (a) and HIF-1α mRNA level (b) in cardiomyocytes. c Western blot analysis of HIF-1α protein level in cardiomyocytes. d LDH release in cardiomyocytes. e The autophagosome puncta of GFP-LC3 by immunofluorescence in cardiomyocytes. Scale bar: 20 μm. f Western blot was performed to examine the protein levels of LC3-I, LC3-II, and Beclin-1 in cardiomyocytes. g 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. a–f **p < 0.01 vs. Control group. g **p < 0.01 vs. Vector group, ^##p < 0.01 vs. si-Ctrl group