Serum extracellular vesicles promote proliferation of H9C2 cardiomyocytes by increasing miR-17-3p

Journal Article · Tue May 15 04:00:00 EDT 2018 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2018.03.157· OSTI ID:23137174

Liu, Zhuyuan ^[1]; Zhang, Zhongrong ^[2]; Yao, Jianhua ^[3]; Xie, Yuan ^[4]; Dai, Qiying ^[1]; Zhang, Yuhui ^[5]; Zhou, Lei ^[1]

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1. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029 (China)
2. Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai 200444 (China)
3. Department of Cardiology, Shanghai Tenth Hospital, Tongji University School of Medicine, Shanghai 200072 (China)
4. Department of Cardiology, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai 200065 (China)
5. State Key Laboratory of Cardiovascular Disease, Heart Failure Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing (China)

Highlights: • Serum extracellular vesicles promotes H9C2 cardiomyocytes proliferation. • miR-17-3p mediates the pro-proliferation effects. • TIMP3 is a target gene of miR-17-3p. Emerging evidence showed that cardiac proliferation played a significant role in the cardiac rehabilitation and repair. Extracellular vesicles (EVs) are known to regulate multiple cell functions, whereas the role of EVs in cardiac proliferation still remains unclear. In this study, we found that serum EVs promoted cell proliferation in rat heart myoblastic H9C2 cells with significantly increased expression level of miR-17-3p. Inhibition of miR-17-3p could decrease H9C2 cells proliferation induced by serum EVs. Additionally, we found that TIMP3 was a target of miR-17-3p in H9C2 cells proliferation and the expression of TIMP3 was downregulated by serum EVs. Meanwhile, inhibition of TIMP3 increased cardiac proliferation. In conclusion, results of our study indicated that serum EVs could promote the proliferation of H9C2 cells via regulating miR-17-3p/TIMP3, which may be a potential therapeutic target for treatment of cardiac injury.

• OSTI ID: 23137174
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 3 Vol. 499; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
CELL PROLIFERATION
HEART
INJURIES
RATS