期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 32, 期 6, 页码 1741-1750出版社
KARGER
DOI: 10.1159/000356608
关键词
Thymic stromal lymphopoietin; Inflammation; Platelets; Acute coronary syndrome
资金
- National Natural Science Foundation of China [3114635]
Background: Thymic stromal lymphopoietin (TSLP) has been shown to be expressed in various inflammatory tissues, such as human atherosclerotic plaques. Many types of myeloid cells involved in atherosclerosis, including mast cells, lymphocytes, dendritic cells and monocytes/macrophages, present TSLP receptors (TSLPR). However, it is unknown whether platelets, which also play important roles in atherothrombosis, express TSLPR. Methods and Results: We applied flow cytometry and western blotting to show that TSLPR was expressed on the surface of human platelets. Following the addition of TSLP to platelets, the expression of CD62P, CD63, PAC-1 and p-Akt as well as aggregation and ATP release were increased significantly. A TSLPR antibody and a PI3K (phosphatidylinositol 3-kinase) enzyme inhibitor (LY294002) significantly inhibited the platelet activation induced by TSLP. The expression of TSLPR, CD62P and CD63 and the increment of the expression of CD62P and CD63 induced by TSLP in the acute coronary syndrome (ACS) group were markedly higher than those in the control group and the stable angina pectoris (SAP) group. The expression and the increment of the expression of CD62P and CD63 induced by TSLP were positively correlated with the expression of TSLPR. Conclusion: Human platelets express functional TSLPR, which can be activated by TSLP to promote platelet activation. TSLP/TSLPR functions via activating the PI3K/AKT pathway, and this signalling pathway may be one of the mechanisms involved in thrombosis in ACS. In coronary disease patients, the determination of TSLPR in platelets may help to identify the risk of ACS. Copyright (C) 2013 S. Karger AG, Basel
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