Regulation of Mitochondria on Platelet Apoptosis and Activation.
10.19746/j.cnki.issn.1009-2137.2023.03.029
- Author:
Ying HU
1
;
Li-Li ZHA
1
;
Ke-Sheng DAI
2
Author Information
1. Medical College of Soochow University, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, Institute of Blood and Marrow Transplantation, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou 215123, Jiangsu Province, China.
2. Medical College of Soochow University, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, Institute of Blood and Marrow Transplantation, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou 215123, Jiangsu Province, China . E-mail: kdai@suda.edu.cn.
- Publication Type:Journal Article
- Keywords:
apoptosis;
platelet;
reactive oxygen species
- MeSH:
Humans;
Blood Platelets/metabolism*;
Antioxidants/pharmacology*;
Mitochondria/physiology*;
Platelet Activation;
Apoptosis;
Membrane Potential, Mitochondrial;
Reactive Oxygen Species/pharmacology*
- From:
Journal of Experimental Hematology
2023;31(3):816-822
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the regulation of mitochondria on platelet apoptosis and activation, and the relationship between platelet apoptosis and activation.
METHODS:Platelets were isolated from peripheral venous blood of healthy volunteers. Cyclosporin A (CsA), which has a protective effect on the function of platelet mitochondria, BAPTA, which can chelate calcium ions across membranes in platelets, and NAC, an antioxidant that reduces the level of intracellular reactive oxygen species, were selected for coincubation with washed platelets, respectively. By flow cytometry, platelet aggregator was used to detect the changes of platelet mitochondrial function and platelet activation indexes after different interventions.
RESULTS:H89, staurosporine, and A23187 led to platelet mitochondrial abnormalities, while CsA could effectively reverse the decline of platelet mitochondrial membrane potential caused by them. Antioxidant NAC could reverse platelet mitochondrial damage correspondingly, and completely reverse platelet shrinkage and phosphatidylserine eversion induced by H89. BAPTA, prostaglandin E1, acetylsalicylic acid and other inhibitors could not reverse the decline of platelet mitochondrial membrane potential.
CONCLUSION:Mitochondrial function plays an important role in platelet apoptosis and activation. Abnormal mitochondrial function causes the imbalance of reduction/oxidation state in platelets, which leads to platelet apoptosis. Platelet apoptosis and activation are independent signal processes.
