Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018
MicroRNA-210 aggravates hypoxia-induced injury in cardiomyocyte H9c2 cells by targeting CXCR4.
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Feng Min, Li Zongqing, Wang Dong, Wang Fang, Wang Chenyan, Wang Chunfang, Ding Faming
Аннотация
BACKGROUND: Myocardial infarction (MI), a leading cause of mortality, is identified as the myocardial necrosis due to prolonged ischemia. Hypoxia, resulting from ischemia, induces cell apoptosis during MI. Since miR-210 is a hypoxia inducible factor, we aimed to explore the functional role of miR-210 in hypoxic H9c2 cells.
METHODS: Hypoxia-induced cell injury was evaluated according to cell viability, apoptosis and expression of apoptosis-associated proteins. miR-210 expression after hypoxia was tested. Then, miR-210 was overexpressed or silenced, and its effects on viability and apoptosis of H9c2 cells under normoxia and hypoxia were measured. Utilizing bioinformatics method, possible target genes of miR-210 were screened, and the interaction between miR-210 and target gene was investigated. Moreover, the effect of co-transfections with microRNAs and small interfering RNAs on hypoxia-induced cell injury as well as the possible involved signaling pathways was also determined.
RESULTS: Hypoxia induced cell injury and up-regulation of miR-210 in H9c2 cells. Hypoxia-induced cell injury was aggravated by miR-210 overexpression but was attenuated by miR-210 suppression. CXC chemokine receptor 4 (CXCR4) was a target gene of miR-210, and CXCR4 inhibition could reverse the effects of miR-210 inhibition on H9c2 cells. Furthermore, the key kinases involved in the SMAD and mTOR signaling pathways were down-regulated by hypoxia, and the down-regulations were reversed by miR-210 suppression through modulating CXCR4.
CONCLUSION: miR-210 was up-regulated in hypoxic H9c2 cells. Suppression of miR-210 attenuated hypoxia-induced cell injury in H9c2 cells by targeting CXCR4, along with activations of the SMAD and mTOR signaling pathways.
METHODS: Hypoxia-induced cell injury was evaluated according to cell viability, apoptosis and expression of apoptosis-associated proteins. miR-210 expression after hypoxia was tested. Then, miR-210 was overexpressed or silenced, and its effects on viability and apoptosis of H9c2 cells under normoxia and hypoxia were measured. Utilizing bioinformatics method, possible target genes of miR-210 were screened, and the interaction between miR-210 and target gene was investigated. Moreover, the effect of co-transfections with microRNAs and small interfering RNAs on hypoxia-induced cell injury as well as the possible involved signaling pathways was also determined.
RESULTS: Hypoxia induced cell injury and up-regulation of miR-210 in H9c2 cells. Hypoxia-induced cell injury was aggravated by miR-210 overexpression but was attenuated by miR-210 suppression. CXC chemokine receptor 4 (CXCR4) was a target gene of miR-210, and CXCR4 inhibition could reverse the effects of miR-210 inhibition on H9c2 cells. Furthermore, the key kinases involved in the SMAD and mTOR signaling pathways were down-regulated by hypoxia, and the down-regulations were reversed by miR-210 suppression through modulating CXCR4.
CONCLUSION: miR-210 was up-regulated in hypoxic H9c2 cells. Suppression of miR-210 attenuated hypoxia-induced cell injury in H9c2 cells by targeting CXCR4, along with activations of the SMAD and mTOR signaling pathways.