Send to

Choose Destination
Eur J Med Res. 2005 May 20;10(5):197-201.

Endothelin-1 induces CD40 but not IL-6 in human monocytes via the proinflammatory transcription factor NF-kappaB.

Author information

Department of Cardiology, University of Heidelberg, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany.


The vasoactive peptide endothelin-1 (ET-1) may contribute to the pathogenesis of atherosclerosis and its acute complications. Because inflammation of the vessel wall is a characteristic feature of atherosclerosis, this study investigated the effect of ET-1 on the proinflammatory transcription factor NF-kappaB in monocytes. Monocyte/macrophages are a major source of inflammatory mediators in atheroma and are located in rupture prone plaque areas. In human monocytes ET-1 caused NF-kappaB activation. Specificity of ET-1-induced NF-kappaB activation was ascertained by supershift and competition experiments. This ET-1 effect was blocked by the ET-A-receptor antagonist BQ-123 but not by the ET-B-receptor antagonist BQ-788. PI-1, a specific inhibitor of the IkappaB-alpha-degrading proteasome complex, also prevented NF-kappaB activation. ET-1 stimulated expression of the proinflammatory molecule CD40 but not of the cytokine IL-6 in a NF-kappaB-dependent manner.


The data demonstrate the ability of ET-1 to activate inflammatory pathways in human monocytes differentially.

[Indexed for MEDLINE]

Supplemental Content

Loading ...
Support Center