Gene interactions and pathways from curated databases and text-mining

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IL10 — VCAM1

Text-mined interactions from Literome

Banning et al., Free Radic Biol Med 2004 : Inhibition of basal and interleukin-1 induced VCAM-1 expression by phospholipid hydroperoxide glutathione peroxidase and 15-lipoxygenase in rabbit aortic smooth muscle cells
Cervera et al., J Neurosci Res 2004 (Brain Infarction...) : UH-treated rats showed smaller infarctions than rats treated with vehicle, as well as higher IL-10 plasma levels and HO-1 brain expression and lower endothelial VCAM-1 induction
Krakauer et al., Immunol Lett 1995 : IL-10 also down-regulated the expression of ICAM-1 and VCAM-1 on IL-1 activated endothelial cells
Deisher et al., Life Sci 1993 (Second Messenger Systems) : Surface protein expression of vascular cell adhesion molecule-1 , endothelial leukocyte adhesion molecule-1, or intercellular adhesion molecule-1, which is induced by tumor necrosis factor, interleukin-1 , and lipopolysaccharide, was not induced by pentoxyfilline, a phosphodiesterase inhibitor, nor by dibutyryl cyclic adenosine monophosphate
Fiehn et al., Immunology 1997 : Selective enhancement of endothelial cell VCAM-1 expression by interleukin-10 in the presence of activated leucocytes ... However, in the presence of phytohaemagglutinin activated PBMC, IL-10 increased the expression on endothelial cells of vascular cell adhesion molecule-1 ( VCAM-1 ) but not of intercellular adhesion molecule-1, E-selectin or major histocompatibility complex ( MHC ) antigens, an effect mediated by PBMC derived soluble factors ... Our results suggest that the relative balance of cytokines produced by infiltrating cells in developing inflammatory lesions may differentially modulate endothelial responsiveness in vivo, and that IL-10 might indirectly stabilize VCAM-1 expression on endothelial cells by affecting the balance of leucocyte derived cytokines in the endothelial environment
Miller et al., J Leukoc Biol 1998 : Utilizing neutralizing antibodies, we show that CD40L mediated tissue factor and thrombomodulin modulation, as well as E-selectin and VCAM-1 upregulation, is independent of tumor necrosis factor alpha, interleukin-1alpha , or interleukin-1beta production