4.6 Article

Expression of toll-like receptors on human platelets

Journal

THROMBOSIS RESEARCH
Volume 113, Issue 6, Pages 379-385

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2004.03.023

Keywords

coronary artery disease; infection; inflammation; thrombosis

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Introduction: Platelets play a crucial role in arterial thrombosis, which is the main cause of acute coronary syndrome. Some mycobacteriums, such as Chlamydia pneumoniae, were associated with progression of atherosclerosis and they are interacted with Toll-like receptors (TLRs), which have been defined as pathogen-associated molecular pattern recognition molecules in innate immunity. In the present study, we examined whether human platelets express TLRs. Materials and methods: Human platelets were obtained from healthy volunteers and the mRNA and protein [eve( of TLRs on platelets and Meg-01 cells, megakaryoblastic cell line, were investigated. Results: Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated that TLR1 and TLR6 mRNA were expressed in platelets and Meg-01 cells. Furthermore, interferon-gamma up-regulated their mRNA levels in dose and time dependent manners after stimuli. Both TLR1 and TLR6 proteins in platelets were detected by Western blotting, and their expression of platelets was more than that of Meg-01 cells. Flow cytometry analysis revealed the expression of TLR1 and TLR6 on the cell surface of Meg-01 cells. Furthermore, immunohistochemical analysis using human coronary thrombi obtained from patients with acute coronary syndrome confirmed the expression of TLR1 and TLR6 on platelets. Conclusion: In summary, we demonstrated that human platelets and Meg-01 cells expressed a family of TLRs for the first time, and our findings indicated that platelets might recognize antigens directly via TLRs. Our findings suggest a possibility that platelets have the ability to recognize the antigens via TLRs and that there are mechanistic relations between infectious inflammation and atherosclerotic vascular diseases. (C) 2004 Elsevier Ltd. All rights reserved.

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