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Endothelin-1 Stimulates Small Artery VCAM-1 Expression through p38MAPK-Dependent Neutral Sphingomyelinase

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  • Medicine

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Endothelin-1 Stimulates Small Artery VCAM-1 Expression through p38MAPK-Dependent Neutral Sphingomyelinase Research Paper J Vasc Res 2012;49:353–362 DOI: 10.1159/000336649 Endothelin-1 Stimulates Small Artery VCAM-1 Expression through p38MAPK-Dependent Neutral Sphingomyelinase Jacqueline Ohanian Simon P. Forman Gideon Katzenberg Vasken Ohanian Cardiovascular Medicine, University of Manchester, Manchester , UK of RMSA with ET-1 (1–100 nmol/l) for 16 h increased VCAM-1 expression, which was inhibited by GW4869 and SB203580. These results indicate that ET-1 stimulates arterial VCAM-1 expression through p38MAPK-dependent activation of neu- tral sphingomyelinases. This suggests a role for sphingolip- ids in ET-1-induced vascular inflammation in cardiovascular disease. Copyright © 2012 S. Karger AG, Basel Introduction Vascular inflammation is associated with the remod- elling of small arteries [1] , a process involved in the devel- opment of hypertension, atherosclerosis and vascular complications of diabetes [1, 2] , and there is now consid- erable evidence linking endothelin-1 (ET-1) to resistance artery inflammation and remodelling [3–6] . ET-1 is a po- tent vasoconstrictor [7] , but it is also pro-inflammatory [6] , inducing vascular cell adhesion molecule (VCAM-1) expression, leukocyte adherence to endothelial cells, smooth muscle cell proliferation and arterial remodelling in vitro [8–11] and in vivo [4, 5, 12, 13] . Furthermore, high plasma ET-1 levels correlate with raised soluble VCAM-1 levels in the blood of hypertensive patients and are asso- Key Words Vascular remodelling � Inflammation � Signal transduction � Endothelial cells � Smooth muscle Abstract Endothelin-1 (ET-1) stimulates vascular cell adhesion mole- cule (VCAM-1) expression, a process associated with arterial remodelling. However, the pathways activated by ET-1 that lead to VCAM-1 expression are not fully understood. It is re- por

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