Gene interactions and pathways from curated databases and text-mining

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OSM — SERPINE1

Text-mined interactions from Literome

Spence et al., Cytokine 2002 (Lung Neoplasms) : Inhibitor studies demonstrated that OSM mediated induction of tPA and PAI-1 mRNAs is largely dependent upon activation of the MEK1/2 pathway
Kasza et al., J Neurochem 2002 : We conclude that OSM and IL-1 regulate the PAI-1 gene expression via up-regulating c-fos levels and subsequent binding of c-fos/c-jun heterodimers to the proximal element of the PAI-1 gene
Rega et al., Circulation 2005 (Inflammation) : We used tissue explants and primary cultures of preadipocytes and adipocytes from human subcutaneous and visceral adipose tissue to investigate whether IL-6 and OSM affect PAI-1 expression in fat ... AG-490, a janus kinase/signal transducer and activator of transcription inhibitor, abolished the OSM dependent PAI-1 induction almost completely
Weiss et al., J Mol Cell Cardiol 2005 : The notion that OSM favors matrix stabilization in the human heart is further supported by our earlier observation that OSM also upregulates PAI-1 , the physiological inhibitor of the protease urokinase-type PA ( u-PA ), which in turn is essential for extracellular proteolysis
Demyanets et al., Am J Physiol Heart Circ Physiol 2007 : The inflammatory cytokine oncostatin M induces PAI-1 in human vascular smooth muscle cells in vitro via PI 3-kinase and ERK1/2 dependent pathways ... A phosphatidylinositol 3-kinase inhibitor and a mitogen activated protein/extracellular signal regulated kinase inhibitor reduced Akt and ERK1/2 phosphorylation, respectively, and abolished OSM induced PAI-1 upregulation ... A janus kinase/signal transducer and activator of transcription inhibitor, a p38 mitogen activated protein kinase inhibitor, or c-Jun NH ( 2 ) -terminal kinase inhibitor I did not inhibit the OSM dependent PAI-1 induction ... We hypothesize that, if the effect of OSM on PAI-1 expression in smooth muscle cells is operative in vivo, it could, via modulation of fibrinolysis and extracellular proteolysis, be involved in the development of vascular pathologies such as plaque progression, destabilization and subsequent thrombus formation, and restenosis and neointima formation
Pourtau et al., Blood Coagul Fibrinolysis 1998 (Arteriosclerosis) : Since oncostatin M dramatically induces fibrinogen biosynthesis by hepatocytes and could be implicated in vascular injury leading to atherosclerosis, we have analyzed the effect of oncostatin M on PAI-1 , vWf and tPA secretion by endothelial cells ... On human umbilical vein endothelial cells, oncostatin M induced an increase in PAI-1 and a decrease in tPA secretion, which could explain the thrombogenicity of oncostatin M on large vessels