Repression of miR-764-5p by enhancing IGF1R and cochaperone CHIP expression in mesenchymal stem cells (MSCs) regulates cardioprotective effects in Aging-Spontaneously Hypertensive rats model

Author:

Huang Chih-Yang1,Barik Parthasarathi2,Kuo Wei-Wen2,Kuo Chia-Hua3,Hsieh Dennis4,Day Cecilia5,Daddam Jayasimharayalu6,Chen Michael7,Padma V. Vijaya8,Shibu Marthandam6

Affiliation:

1. Tzu Chi University of Science and Technology

2. China Medical University

3. University of Taipei

4. Chung Shan Medical University Hospital

5. Mei Ho University

6. Hualien Tzu Chi Hospital

7. Buddhist Tzu Chi General Hospital

8. Bharathiar University

Abstract

Abstract Age-associated cardiovascular disease (CVD) progression is marked by increased misfolded proteins and reduced growth factor receptor activity. Evidence links the co-chaperone CHIP and insulin-like growth factor-1 receptor (IGF1R) to stem cell dynamics and function through miR-764-5p in rat adipose-derived stem cells (rADSCs) remains largely unknown. We observed that short-term hypoxia (6 h) downregulated miR-764-5p in rADSCs, while normoxia conditions led to miR-764-5p upregulation, targeting the 3' UTR region of IGF1R and STUB1/CHIP. qRT-PCR confirmed altered mRNA expression. Overexpression of anti-miR-764-5p enhanced rADSC survival via CHIP and IGF1R upregulation, while miR-764-5p mimic increased ROS generation and apoptosis. HIF1α transcription factor downregulated miR-764-5p under short-term hypoxia. Administering rADSCsanti−miR−764−5p in aging-spontaneously hypertensive rats (SHR) via tail-vein injection demonstrated cardioprotective effects, reducing cardiac hypertrophy, fibrosis, and apoptosis and it could be the potential to act as a regenerative medicine. In conclusion, suppressing miR-764-5p enhances IGF1R expression and CHIP activity in rADSCs, mitigating cardiac hypertrophy and remodeling in the aging-SHR model.

Publisher

Research Square Platform LLC

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