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INS — VCAM1

Text-mined interactions from Literome

De Mattia et al., Diabetologia 1999 (Diabetes Mellitus, Type 2) : Effects of insulin on in vitro vascular cell adhesion molecule-1 expression and in vivo soluble VCAM-1 release ... To evaluate the effects of insulin on vascular cell adhesion molecule-1 expression by cultured human vascular endothelial cells and soluble vascular cell adhesion molecule-1 release in vivo
Madonna et al., Diabetologia 2004 (Arteriosclerosis...) : Insulin enhances vascular cell adhesion molecule-1 expression in human cultured endothelial cells through a pro-atherogenic pathway mediated by p38 mitogen activated protein-kinase ... In the absence of cytotoxicity, wortmannin significantly potentiated the effect of insulin alone on VCAM-1 surface expression and monocytoid cell adhesion, whereas SB-203580 ( 10 ( -6 ) mol/l ) completely abolished such effects
Madonna et al., Int J Immunopathol Pharmacol 2007 : The prominent role of p38 mitogen activated protein kinase in insulin mediated enhancement of VCAM-1 expression in endothelial cells ... We previously showed that insulin increases monocyte-endothelial interactions and the endothelial expression of the pro-atherogenic vascular cell adhesion molecule-1 ( VCAM-1 ) ... The aim of this study is to examine molecular mechanisms involved in the effect of insulin on VCAM-1 expression ... At pathophysiological concentrations ( 10 ( -9 ) -10 ( -7 ) M ), insulin selectively induced VCAM-1 expression ... Gene silencing by small interfering RNA significantly reduced the expression of p38MAP kinase, and this was accompanied by suppression of insulin stimulated VCAM-1 expression ... Co-treatment of HUVEC with insulin and SB202190 strongly reverted the stimulatory effect of insulin on NF-KB activation, thus establishing a link between NF-KB activation and p38MAPkinase mediated induction of VCAM-1 by insulin
Madonna et al., Biochim Biophys Acta 2008 : At pathophysiological/pharmacological concentrations ( 10 ( -9 ) -10 ( -7 ) mol/L ), insulin selectively induced VCAM-1 expression and potentiated the effects of TNF-alpha andLPS, effects reverted by the proteasome inhibitor lactacystin
Li et al., Endocrinology 2009 : Insulin receptor small interfering RNA knockdown abolished insulin stimulated increases of ICAM-1 but not VCAM-1 ... Conversely, IGF-I receptor blockade with either a neutralizing antibody or specific small interfering RNA eliminated insulin induced VCAM-1 but not ICAM-1 production