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MMP2 — PLAU
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Lau et al., Cardiovasc Res 1999
:
Epithelioid SMC, but not swirling SMC, secreted
MMP-2 in
response to
uPA and tPA
Menshikov et al., Biochem J 2002
:
In the present study, the
role of
uPA in regulating
matrix metalloproteinase ( MMP ) expression and release by the monocyte cell line THP-1 was investigated
Kim et al., J Cell Biochem 2003
(Neovascularization, Pathologic) :
In conclusion, these data suggest that genistein, apigenin, and 3-hydroxyflavone inhibit in vitro angiogenesis, in part via preventing VEGF/bFGF induced MMP-1 and
uPA expression and the
activation of
pro-MMP-2 , and via modulating their inhibitors, TIMP-1 and -2, and PAI-1
Siconolfi et al., J Neurosci Res 2003
:
Both tPA and uPA activate some matrix metalloproteases ( MMPs ), indirectly via plasminogen activation or directly, such as the
uPA activation of
MMP-2
Stempien-Otero et al., J Biol Chem 2006
(Fibrosis) :
We hypothesized that : 1 ) macrophage accumulation and cardiac fibrosis in SR-uPA+/o mice are dependent on localization of uPA by the uPA receptor (uPAR) ; 2 ) activation of plasminogen by
uPA and subsequent
activation of transforming growth factor-beta1 ( TGF-beta1 ) and
matrix metalloproteinase (MMP)-2 and -9 by plasmin are critical pathways through which uPA expressing macrophages accumulate in the heart and cause fibrosis ; and 3 ) uPA induced cardiac fibrosis can be attenuated by treatment with verapamil
Quemener et al., Cancer Res 2007
(Breast Neoplasms...) :
EMMPRIN expressing cells also exhibited enhanced invasive potential in vitro, and the use of amiloride (
uPA inhibitor ) and marimastat (
MMP inhibitor ) showed that the two proteolytic systems reduced alone and in combination the invasive potential mediated through EMMPRIN
Cheng et al., Mol Cell Biochem 2009
:
Here, we show that LPS challenge increased the protein levels of
uPA , MMP-2 and MMP-9, and
induced the activity of
MMP-2 and MMP-9 in H9c2 cardiomyoblasts
Maupas-Schwalm et al., Cell Signal 2009
:
We report that
uPA , as well as its catalytically inactive N-amino fragment ATF,
triggers the sequential activation of
MMP-2 , NSMase-2 and ERK1/2 in ECV304 cells that are required for uPA induced ECV304 proliferation, as assessed by the inhibitory effect of Marimastat ( a MMP inhibitor ), MMP-2-specific siRNA, MMP-2 defect, and NSMase-specific siRNA