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The MicroRNA-210/Casp8ap2 pathway alleviates hypoxia-induced injury in myocardial cells by regulating apoptosis and autophagy
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  • kunsheng li,
  • jun pan,
  • qiuchang li,
  • shiliang li,
  • kai li,
  • yongqing cheng,
  • lin chai,
  • chao li,
  • junling li,
  • zhikun fu,
  • dongjin wang,
  • yang bai
kunsheng li
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qiuchang li
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shiliang li
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yongqing cheng
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junling li
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dongjin wang
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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

Peer review status:Published

21 Oct 2020Published in The Heart Surgery Forum volume 23 issue 6 on pages E797-E802. 10.1532/hsf.3173