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- Title
Oxidized Low-Density Lipoprotein-Dependent Platelet-Derived Microvesicles Trigger Procoagulant Effects and Amplify Oxidative Stress.
- Authors
Hua Wang; Zhi-Hao Wang; Jing Kong; Meng-Yun Yang; Gui-Hua Jiang; Xu-Ping Wang; Ming Zhong; Yun Zhang; Jing-Ti Deng; Wei Zhang
- Abstract
The fundamental mechanisms that underlie platelet activation in atherothrombosis are still obscure. Oxidative stress is involved in central features of atherosclerosis. Platelet-derived microvesicles (PMVs) could be important mediators between oxidative stress and platelet activation. CD36 could be a receptor of PMVs, thus generating a PMV-CD36 complex. We aimed to investigate the detailed pathway by which oxidative damage contributes to platelet activation by the PMV-CD36 complex. We found that oxidized low-density lipoprotein stimulated the generation of PMVs. PMVs enhanced normal platelet activation, as assessed by the expression of integrin αIIbβ3, secretion of soluble P-selectin and platelet aggregation, but CD36-deficient platelets were not activated by PMVs. The function of the PMV-CD36 complex was mediated by the MKK4/JNK2 signaling axis. Meanwhile, PMVs increased the level of 8-iso-prostaglandin-F2α, a marker of oxidative stress, in a CD36- and phosphatidylserine-dependent manner. We concluded that PMVs are important mediators between oxidative stress and platelet activation. PMVs and CD36 may be effective targets for preventing platelet activation in cardiovascular diseases.
- Subjects
LIPOPROTEINS; BLOOD platelets; PLATELET-derived growth factor; OXIDATIVE stress; INTEGRINS
- Publication
Molecular Medicine, 2012, Vol 18, Issue 2, p159
- ISSN
1076-1551
- Publication type
Article
- DOI
10.2119/molmed.2011.00295