Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94

Ma,Jian‑Lin; Guo,Wen‑Ling; Chen,Xue‑Mei

doi:10.3892/mmr.2018.8375

Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94

Authors:
- Jian‑Lin Ma
- Wen‑Ling Guo
- Xue‑Mei Chen
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Affiliations: Department of Emergency, Binzhou City Central Hospital, Binzhou, Shandong 251700, P.R. China, Department of Obstetrics, Binzhou City Central Hospital, Binzhou, Shandong 251700, P.R. China
Published online on: January 5, 2018 https://doi.org/10.3892/mmr.2018.8375
Pages: 4181-4186
Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNA (miR)-150 has been demonstrated to protect the heart from ischemic injury. However, the protective effect of miR‑150 in hypoxia‑injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR‑150 and the underlying molecular mechanisms of miR‑150 in hypoxia‑induced cardiomyocyte apoptosis. Using the hypoxia model of human cardiomyocytes (HCMs) in vitro, it was demonstrated that miR‑150 was markedly inhibited in HCMs after hypoxia treatment. Overexpressing miR‑150 significantly decreased hypoxia‑induced HCM death and apoptosis. In addition, GRP94 was revealed to be a direct target of miR‑150. Additionally, GRP94 was demonstrated to be involved in hypoxia‑induced HCM apoptosis, and the protein expression levels of GRP94 were increased in HCMs in the presence of hypoxia. These findings demonstrated that miR‑150 is involved in hypoxia‑mediated gene regulation and apoptosis in HCMs. Furthermore, GRP94 knockout increased the cell viability of hypoxia‑impaired HCMs with miR‑150 mimic or miR‑150 inhibitor transfection. In conclusion, miR‑150 may serve a protective role in cardiomyocyte hypoxia injury, and the underlying mechanism was mediated, at least partially, by inhibiting GRP94 expression. These findings may provide a novel insight for the therapy of hypoxia-induced myocardial I/R injury.

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