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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