Mechanism of CINC-1 production from gastric epithelial cells stimulated with TNF-α

被引：0

作者：

Handa, O ^{[1
]}

Naito, Y ^{[1
]}

Takagi, T ^{[1
]}

Ueda, M ^{[1
]}

Ishikawa, T ^{[1
]}

Imamoto, E ^{[1
]}

Tomatsuri, N ^{[1
]}

Uchiyama, K ^{[1
]}

Shimozawa, M ^{[1
]}

Katada, K ^{[1
]}

Ueda, T ^{[1
]}

Kokura, S ^{[1
]}

Ichikawa, H ^{[1
]}

Yoshida, N ^{[1
]}

Yoshikawa, T ^{[1
]}

Gediminas, C ^{[1
]}

Kvietys, PR ^{[1
]}

机构：

[1] Lawson Hlth Res Inst, Vasc Cell Biol Inflammat Program, London, ON, Canada

来源：

XI BIENNIAL MEETING OF THE SOCIETY FOR FREE RADICAL RESEARCH INTERNATIONAL | 2002年

关键词：

D O I：

暂无

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

CINC-1 has been suggested to play a role as a mediator of inflammatory reactions with neutrophil infiltration in rats. In this study, e investigate the mechanism of CINC-1 production from rat gastric mucosal cell (RGM-1) in response to TNF-alpha stimulation in vitro. TNF-alpha stimulation results in, 1) up-regulation of CINC-1 mRNA and protein, 2) NF-kappaB p65 activation, and 3) increase in cH(2)DCF-DA oxidation. These changes were reversed by several inhibitors against NF-kappaB activation, endogenous reactive oxygen production. In conclusion, TNF-alpha-induced CINC-1 production from RGM-1 cells depends on NF-kappaB and oxidative stress.

引用

页码：347 / 350

页数：4

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