Objective: We investigate the effect of long non-coding RNA H19 in acute myocardial infarction (AMI) and the underlying mechanism.
Materials and methods: C57BL/6 mice were subjected to AMI and injected with lentivirus pcDNA-H19. After AMI procedures for 3 weeks, cardiac function was detected by echocardiography. The infarct size was stained by triphenyltetrazolium chloride. H19 expression in mice was measured by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Protein expressions of LC3, Beclin-1, and ATG-7 in mice were measured by Western blot.
Results: Our results indicated that H19 expression was significantly downregulated in the infarcted myocardium. Overexpression of H19 after injection with pcDNA-H19 in mice could reduce infarct size and improve cardiac function through upregulating the ratio of LC3-II/I and expressions of Beclin-1 and ATG-7.
Conclusions: Overexpression of H19 could protect AMI in mice via activating autophagy.