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Functional role and molecular mechanisms underlying prohibitin 2 in platelet mitophagy and activation.

Authors
  • Hu, Long-Long1
  • Zou, Kai1
  • Chen, Yuan1
  • Wu, Li-Juan1
  • Cao, Jie1
  • Xiong, Xiao-Ying1
  • Wang, Ling2
  • Cheng, Xiao-Shu1
  • Xiao, Qing-Zhong3
  • Yang, Ren-Qiang1
  • 1 Department of Cardiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. , (China)
  • 2 Medicine Lab, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. , (China)
  • 3 Department of Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Type
Published Article
Journal
Molecular Medicine Reports
Publisher
Spandidos Publications
Publication Date
May 01, 2021
Volume
23
Issue
5
Identifiers
DOI: 10.3892/mmr.2021.12023
PMID: 33760146
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Platelet mitophagy is a major pathway involved in the clearance of injured mitochondria during hemostasis and thrombosis. Prohibitin 2 (PHB2) has recently emerged as an inner mitochondrial membrane receptor involved in mitophagy. However, the mechanisms underlying PHB2‑mediated platelet mitophagy and activation are not completely understood. PHB2 is a highly conserved inner mitochondrial membrane protein that regulates mitochondrial assembly and function due to its unique localization on the mitochondrial membrane. The present study aimed to investigate the role and mechanism underlying PHB2 in platelet mitophagy and activation. Phorbol‑12‑myristate‑13‑acetate (PMA) was used to induce MEG‑01 cells maturation and differentiate into platelets following PHB2 knockdown. Cell Counting Kit‑8 assays were performed to examine platelet viability. Flow cytometry was performed to assess platelet mitochondrial membrane potential. RT‑qPCR and western blotting were conducted to measure mRNA and protein expression levels, respectively. Subsequently, platelets were exposed to CCCP and the role of PHB2 was assessed. The results of the present study identified a crucial role for PHB2 in platelet mitophagy and activation, suggesting that PHB2‑mediated regulation of mitophagy may serve as a novel strategy for downregulating the expression of platelet activation genes. Although further research into mitophagy is required, the present study suggested that PHB2 may serve as a novel therapeutic target for thrombosis‑related diseases due to its unique localization on the mitochondrial membrane.

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