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pubmed-article:19450557pubmed:abstractTextBiomechanical stress modulates vascular tone, vascular remodelling and the spatial localisation of atherosclerotic plaques. Inflammatory cytokines, such as TNF-alpha, regulate expression of genes that impair the function of endothelial cells. This study investigates the combinatory effect of different biomechanical stresses and TNF-alpha on the expression of endothelial anti- and prothrombotic genes. Human umbilical vein endothelial cells were exposed to TNF-alpha and different levels of static/pulsatile tensile stress or shear stress. The response in endothelial cells to TNF-alpha was not modulated by tensile stress. However, shear stress was a more potent stimulus. Shear stress counteracted the cytokine-induced expression of VCAM-1, and the cytokine-suppressed expression of thrombomodulin and eNOS. Shear stress and TNF-alpha additively induced PAI-1, whereas shear stress blocked the cytokine effect on t-PA and u-PA. A flow profile characterized by high laminar shear stress seems to render the endothelial cell more resistant to inflammatory stress.lld:pubmed
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pubmed-article:19450557pubmed:year2009lld:pubmed
pubmed-article:19450557pubmed:articleTitleInfluence of TNF-alpha and biomechanical stress on endothelial anti- and prothrombotic genes.lld:pubmed
pubmed-article:19450557pubmed:affiliationClinical Experimental Research Laboratory, Sahlgrenska University Hospital/Ostra, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.lld:pubmed
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