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Cardiovascular Research 2001 49(1):189-199; doi:10.1016/S0008-6363(00)00220-0
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Transient interaction of activated platelets with endothelial cells induces expression of monocyte-chemoattractant protein-1 via a p38 mitogen-activated protein kinase mediated pathway

Implications for atherogenesis

Timm Dickfelda, Ernst Lengyelc, Andreas E Mayb, Steffen Massbergb, Korbinian Brandd, Sharon Paged, Christiane Thielenb, Kirsten Langenbrinkb and Meinrad Gawazb,*

aMedical Department, Duke University, Durham, NC, USA
b1. Medizinische Klinik Klinikum rechts der Isar and Deutsches Herzzentrum, Technische Universität, Lazarettstrasse 36, 80636 Munich, Germany
cFrauenklinik Technische Universität, Munich, Germany
dInstitut für Klinische Chemie and Pathobiochemie, Technische Universität, Munich, Germany

* Corresponding author. Tel.: +49-89-1218-4012; fax: +49-89-1218-4003 gawaz{at}dhm.mhn.de

Objective: Activated platelets induce alterations of chemotactic and adhesive properties of endothelial cells, a critical initial step in atherogenesis. We investigated the effect of transient interaction of activated platelets with cultured human umbilical vein endothelial cells (HUVECs) on secretion of monocyte chemoattractant protein-1 (MCP-1), a key molecule in monocyte chemotaxis and transmigration. Methods and results: Transient interaction of {alpha}-thrombin-activated platelets with endothelial cells for 10–120 min substantially induced endothelial secretion of MCP-1, monocyte chemotaxis and adhesion to HUVECs. Platelet-induced secretion of MCP-1 and monocyte–endothelium adhesion was reduced by the MAP kinase p38-specific inhibitor SB203580, but not by other kinase inhibitors including PD98059, wortmannin, or rapamycin. In addition, activated platelets induced transcription of a luciferase reporter construct containing a MCP-1 promotor, an effect that could be inhibited by SB203580. Overexpression of dominant-negative mutants of MAP kinase p38, CSBP2-(D168A) and CSBP2-(T180E,Y182E) reduced platelet-induced expression of MCP-1. Conclusions: Activation of the p38 MAP kinase and consecutive endothelial secretion of MCP-1 induced through transient interaction of activated platelets might play an important role in atherogenesis.

KEYWORDS Platelets; Endothelial function; Atherosclerosis; Complement activation


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