Skip Navigation

Cardiovascular Research 2001 49(1):189-199; doi:10.1016/S0008-6363(00)00220-0
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Dickfeld, T.
Right arrow Articles by Gawaz, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dickfeld, T.
Right arrow Articles by Gawaz, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

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


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.