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Cardiovascular Research 2002 56(2):284-292; doi:10.1016/S0008-6363(02)00600-4
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

MCP-1 induces activation of MAP-kinases ERK, JNK and p38 MAPK in human endothelial cells

Martina Werle, Ulrike Schmal, Katharina Hanna and Jörg Kreuzer*

Innere Medizin III, Universität Heidelberg, Bergheimer Strasse, 58 69115 Heidelberg, Germany

joerg_kreuzer{at}med.uni-heidelberg.de

* Corresponding author. Tel.: +49-6221-568-676; fax: +49-6221-565-515.

Activation of vascular endothelial cells (ECs) plays an important pathogenic role in the development of atherosclerosis. Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant of monocytes. Besides induction of monocyte recruitment, it has been suggested that MCP-1 can also affect the cellular responses of ECs. We investigated whether MCP-1 activated the three major mitogen activated protein (MAP)-kinases extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK) and p38 MAPK. Stimulation of ECs with MCP-1 induced a time- and concentration-dependent activation of all three MAP-kinases, concentrations as low as 0.1 ng/ml were sufficient for this mechanism. MCP-1 also induced secretion of matrix metalloproteinase (MMP)-2 which along with ERK activation was inhibited by PD098059. The results demonstrate that MCP-1 can lead to direct activation of MAP kinases together with induction of MMP2 in ECs. Our data thus propose a new mechanism for the proatherogenic effect of MCP-1.

KEYWORDS EC, endothelial cells; MCP-1, monocyte chemoattractant protein-1; ERK 1/2, extracellular signal-regulated kinase; JNK, c-Jun amino terminal kinase; PTX, pertussis toxin; CTX, cholera toxin; MMP, matrixmetalloproteinase


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