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SHP-2-Erk signaling regulates concanavalin A-dependent production of TIMP-2.

Abstract：

:To search for the signaling critical for the production of tissue inhibitor of metalloproteinase-2 (TIMP-2), we investigated the role of SHP-2 in TIMP-2 production with Concanavalin A (Con A)-treated cells. In wild-type fibroblasts, Con A-treatment dramatically activated TIMP-2 production. In contrast, production of TIMP-2 in response to Con A-treatment was severely impaired in cells expressing mutant SHP-2 whose 65 amino acids in the SH2-N domain were deleted. Con A-treatment activated dual signaling pathways, Erk and p38, in a SHP-2-dependent manner. Pretreatment of wild-type cells with U0126, a potent inhibitor of MEK1, significantly inhibited the production of TIMP-2, whereas SB203580, a specific inhibitor for p38, could not. Finally, expression of exogenous wild-type SHP-2 in SHP-2 mutant cells clearly rescued Erk activation and TIMP-2 production in response to Con A-treatment. Taken together, our results strongly suggest that SHP-2 plays a critical role as a positive modulator for the production of TIMP-2 via MEK1-Erk signaling in fibroblasts.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Biswas MH,Hasegawa HH,Rahman MA,Huang P,Mon NN,Ruhul Amin AR,Senga T,Kannagi R,Hamaguchi M

doi

10.1016/j.bbrc.2006.07.173

subject

Has Abstract

pub_date

2006-09-29 00:00:00

pages

1145-9

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)01751-7

journal_volume

348

pub_type

杂志文章

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