The MicroRNA-210/Casp8ap2 pathway alleviates hypoxia-induced injury in
myocardial cells by regulating apoptosis and autophagy
Abstract
Abstract Aim: This study was conducted to investigate the role of the
miR-210/Caspase8ap2 pathway in apoptosis and autophagy in hypoxic
myocardial cells. Methods: The miR-control, miR-210 mimic and miR-210
inhibitor were transfected into rat myocardial H9C2 cells. The
transfection efficiency of exogenous miR-210 was determined by
quantitative reverse-transcription polymerase chain reaction (qRT-PCR).
H9C2 cells were then treated with CoCl2 for 24, 48 and 72 h to generate
a myocardial injury model. The apoptosis of H9C2 cells was assessed by
flow cytometry. Additionally, a western blot assay was used to determine
the expression of the autophagy-associated proteins light chain 3 (LC3),
p62 and Beclin-1, and apoptosis-associated proteins Caspase8ap2, cleaved
caspase 8 and cleaved caspase 3. Results: We determined that a 48 h
hypoxia treatment duration in H9C2 cardiomyocytes induced myocardial
injury. Additionally, the overexpression of miR-210 significantly
inhibited cell apoptosis. MiR-210 suppressed autophagy by upregulating
p62 and downregulating LC3II/I in hypoxic H9C2 cells. Since Caspase8ap2
was a putative target of miR-210, miR-210 mediated apoptosis and
autophagy of H9C2 cells via suppressing Caspase8ap2. Furthermore, the
expression of caspase 8, caspase 3 and Beclin-1 were decreased in
response to miR-210. Conclusion: miR-210 exhibits anti-apoptosis and
anti-autophagy effects, which alleviate myocardial injury in response to
hypoxia. Keywords: miR-210; Caspase8ap2; myocardial injury; hypoxia;
apoptosis; autophagy