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

Published on Mar 24, 2021in Molecular Medicine Reports2.1
· DOI :10.3892/MMR.2021.12023
Longlong Hu1
Estimated H-index: 1
(NCU: Nanchang University),
Kai Zou (NCU: Nanchang University)+ 7 AuthorsRenqiang Yang4
Estimated H-index: 4
(NCU: Nanchang University)
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.
Cited By2
#1Harriet E. Allan (QMUL: Queen Mary University of London)H-Index: 4
#2Melissa A. Hayman (QMUL: Queen Mary University of London)H-Index: 3
Last. Manuel Mayr (BHF: British Heart Foundation)H-Index: 81
view all 13 authors...
Background null Platelets circulate in the blood of healthy individuals for approximately 7-10 days regulated by finely balanced processes of production and destruction. As platelets are anucleate we reasoned that their protein composition would change as they age and that this change would be linked to alterations in structure and function. null Objective null To isolate platelets of different ages from healthy individuals to test the hypothesis that changes in protein content cause alterations...