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Publications

Journal Article Epublish

PubMed: 41313493 DOI: 10.1007/s11033-025-11298-1

The role of Mir-365-5p in regulating NF2-Mediated apoptosis and ROS production in hypoxic cardiomyoblasts.

Mol Biol Rep 53(1):137

Authors: Chih-Hsueh Lin, Wei-Yun Wang, Bruce Chi-Kang Tsai, Wei-Wen Kuo, Chia-Hua Kuo, Kuan-Ho Lin, Tsung-Jung Ho, Pei-Ying Pai, Dennis Jine-Yuan Hsieh, Chih-Yang Huang, Shinn-Zong Lin

Affiliations

  • School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan.
  • Department of Family Medicine, China Medical University Hospital, Taichung, Taiwan.
  • Division of Geriatric Medicine, China Medical University Hospital, Taichung, Taiwan.
  • Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, 970, Taiwan.
  • Department of Biological Science and Technology, College of Life Sciences, China Medical University, Taichung, Taiwan.
  • Ph.D. Program for Biotechnology Industry, China Medical University, Taichung, Taiwan.
  • School of Pharmacy, China Medical University, Taichung, Taiwan.
  • Laboratory of Exercise Biochemistry, The Education University of Hong Kong, New Territories, Hong Kong. School of Physical Education and Sports Science, Soochow University, Suzhou, Jiangsu, China. Department of Movement Sciences and Sports Training, School of Sport Sciences, University of Jordan, Amman, Jordan.
  • Department of Emergency Medicine, China Medical University Hospital, Taichung, Taiwan.
  • Department of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • Integration Center of Traditional Chinese and Modern Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • Division of Cardiovascular Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan.
  • Department of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, 402, Taiwan.
  • Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan.
  • Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, 970, Taiwan. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan. Department of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan.
  • Bioinnovation Center, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
  • Department of Neurosurgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, 970, Taiwan.

Abstract

BACKGROUND

Prolonged hypoxia is known to induce reactive oxygen species (ROS) accumulation, leading to cellular damage, particularly in cardiac cells. MicroRNAs (miRNAs) have emerged as key regulators in cellular responses to hypoxia. This study investigated the role of miR-365-5p in hypoxia-induced injury in H9c2 cardiomyoblasts and explored the potential protective effects of bioactive compounds derived from the Jing Si herbal tea.

METHODS AND RESULTS

Microarray analysis was employed to identify differentially expressed miRNAs in H9c2 cells subjected to 24-hour hypoxic conditions. Among several candidates, mir-365-5p was found to be significantly downregulated, correlating with the upregulation of neurofibromin 2 (NF2), a known regulator of apoptotic signaling pathways. Functional studies using a mir-365-5p mimic revealed that NF2 expression was suppressed, ROS accumulation was decreased, and intrinsic apoptosis was attenuated. Similarly, NF2 knockdown via siRNA recapitulated the protective effects of the mir-365-5p mimic under hypoxic conditions. In parallel, high-performance liquid chromatography (HPLC) was utilized to isolate three individual compounds from Jing Si herbal tea. Treatment with these compounds prevented the hypoxia-induced downregulation of mir-365-5p, suggesting a mechanism for their cardioprotective action.

CONCLUSIONS

The mir-365-5p served as a crucial modulator of hypoxia-induced oxidative stress and apoptosis in H9c2 cardiomyoblasts through the regulation of NF2. Compounds derived from Jing Si herbal tea may exert cardioprotective effects by sustaining mir-365-5p expression under hypoxic conditions. These findings highlight the therapeutic potential of targeting the mir-365-5p/NF2 axis in cardiac injury.

MeSH

Cells, Tea, Molecular Biology, Micrornas, Hypoxia, Therapeutics, Apoptosis, Teas, Herbal