Abstract
BackgroundMetabolic syndrome (MetS) is a common challenge in the world, and the platelet activation is enhanced in MetS patients. However, the fundamental mechanism that underlies platelet activation in MetS remains incompletely understood. Endothelial cells are damaged seriously in MetS patients, then they release more endothelial microparticles (EMPs). After all, whether the EMPs participate in platelet activation is still obscure. If they were, how did they work?ResultsWe demonstrated that the levels of EMPs, PMPs (platelet derived microparticles) and microparticle-carried-PDI activity increased in MetS patients. IR endothelial cells released more EMPs, the EMP-PDI was more activated. EMPs can enhance the activation of CD62P, GPIIb/IIIa and platelet aggregation and this process can be partly inhibited by PDI inhibitor such as RL90 and rutin. Activated platelets stimulated by EMPs expressed more PDI on cytoplasm and released more PMPs.Materials and MethodsWe obtained plasma from 23 MetS patients and 8 normal healthy controls. First we built insulin resistance (IR) model of human umbilical vein endothelial cells (HUVECs), and then we separated EMPs from HUVECs culture medium and used these EMPs to stimulate platelets. Levels of microparticles, P-selectin(CD62P), Glycoprotein IIb/IIIa (GPIIb/IIIa) were detected by flow cytometry and levels of EMPs were detected by enzyme-linked immunosorbent assay (ELISA). The protein disulfide isomerase (PDI) activity was detected by insulin transhydrogenase assay. Platelet aggregation was assessed by turbidimetry.ConclusionEMPs can promote the activation of GPIIb/IIIa in platelets and platelet aggregation by the PDI which is carried on the surface of EMPs.
Highlights
Metabolic syndrome (MetS) caused by insulin resistance (IR) induces hyperinsulinemia and results in a group of diseases that can cause the atherosclerosis [1]
We demonstrated that the levels of endothelial microparticles (EMPs), PMPs and microparticle-carried-protein disulfide isomerase (PDI) activity increased in MetS patients
EMPs can promote the activation of GPIIb/IIIa in platelets and platelet aggregation by the PDI which is carried on the surface of EMPs
Summary
MetS caused by IR induces hyperinsulinemia and results in a group of diseases that can cause the atherosclerosis [1]. MetS accelerates the risk of type 2 diabetes (T2DM) and cardiovascular disease considerably and it is a major cause of thrombosis, which can potentially lead to cardiocerebrovascular diseases and is related to cancer [2,3,4]. Platelet activation is a process of signaling cascade. The mechanism of how platelets are activated in the early process in MetS is unclear. Metabolic syndrome (MetS) is a common challenge in the world, and the platelet activation is enhanced in MetS patients. The fundamental mechanism that underlies platelet activation in MetS remains incompletely understood. Endothelial cells are damaged seriously in MetS patients, they release more endothelial microparticles (EMPs). Whether the EMPs participate in platelet activation is still obscure.
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