MicroRNA‑194‑5p attenuates hypoxia/reoxygenation‑induced apoptosis in H9C2 cardiomyocytes by inhibiting the over‑activation of RAC1 protein

Li,Cuie; Li,Yinghua; Li,Yanping; Wang,Yudi; Teng,Yirong; Hao,Yinglu

doi:10.3892/mmr.2022.12920

MicroRNA‑194‑5p attenuates hypoxia/reoxygenation‑induced apoptosis in H9C2 cardiomyocytes by inhibiting the over‑activation of RAC1 protein

Authors:
- Cuie Li
- Yinghua Li
- Yanping Li
- Yudi Wang
- Yirong Teng
- Yinglu Hao
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Affiliations: Department of Geriatrics, The 6th Affiliated Hospital of Kunming Medical University, The People's Hospital of Yuxi City, Yuxi, Yunnan 653100, P.R. China, Department of General Practice, The 6th Affiliated Hospital of Kunming Medical University, The People's Hospital of Yuxi City, Yuxi, Yunnan 653100, P.R. China, Department of Cardiology, The 6th Affiliated Hospital of Kunming Medical University, The People's Hospital of Yuxi City, Yuxi, Yunnan 653100, P.R. China
Published online on: December 20, 2022 https://doi.org/10.3892/mmr.2022.12920
Article Number: 33
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ras‑related C3 botulinum toxin substrate 1 (RAC1), a member of the Rac family of guanosine triphosphate phosphohydrolases, has been suggested to be a regulator of myocardial injury during ischemia and reperfusion (I/R). Whether microRNAs (miRs) are involved in the regulation of the aforementioned process remains to be elucidated. In the present study, an in vitro model of H9C2 cardiomyocytes was used to establish the overexpression of RAC1 following hypoxia and reoxygenation (H/R). Overexpression of RAC1 in H/R‑cultured cardiomyocytes could lead to cellular accumulation of reactive oxygen species (ROS) and facilitate the induction of apoptosis of H9C2 cardiomyocytes during H/R. Subsequent bioinformatic analysis indicated that RAC1 was the target of miRNA‑194‑5p. Further experiments showed that miR‑194‑5p attenuated the accumulation of cellular ROS and alleviated the induction of apoptosis of H9C2 cardiomyocytes caused by H/R, which was accompanied by the reduction in the expression levels of the RAC1 protein. Taken together, these results indicated that upregulation of miR‑194‑5p may function as a self‑regulated cardioprotective response against RAC1‑mediated ROS accumulation and cardiomyocyte apoptosis. Exogenous administration of miR‑194‑5p may be a novel target to ameliorate I/R injury‑induced myocardial apoptosis.

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