Oxidative stress induces gastric epithelial permeability through claudin-3

被引：88

作者：

Hashimoto, Kayo ^{[1
]}

Oshima, Tadayuki ^{[1
]}

Tomita, Toshihiko ^{[1
]}

Kim, Yongmin ^{[1
]}

Matsumoto, Takayuki ^{[2
]}

Joh, Takashi ^{[3
]}

Miwa, Hiroto ^{[1
]}

机构：

[1] Hyogo Med Univ, Dept Internal Med, Div Upper Gastroenterol, Nishinomiya, Hyogo 6638501, Japan

[2] Hyogo Med Univ, Dept Internal Med, Div Lower Gastroenterol, Nishinomiya, Hyogo 6638501, Japan

[3] Nagoya City Univ, Grad Sch Med Sci, Dept Internal Med & Bioregulat, Nagoya, Aichi 4678601, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 376卷 / 01期

关键词：

tight junction; rebamipide; permeability; claudin-3; siRNA;

D O I：

10.1016/j.bbrc.2008.08.140

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：

Although reactive oxygen species have been implicated as mediators of gastrointestinal injury, their influence on the function of gastric epithelial tight junctions (TJs), which create a paracellular permeability barrier, needs to be fully investigated. H2O2 exposure to MKN28 gastric epithelial monolayers caused a significant decrease in trans-epithelial electrical resistance (TEER) and a significant increase in dextran permeability. Oxidant-mediated gastric epithelial permeability was significantly attenuated by a radical scavenger, rebamipide. H2O2 decreased the amount of claudin-3 protein but not claudin-4, -7, and JAM-A. Rebamipide significantly attenuated H2O2-induced decrease in claudin-3 protein. Small interfering RNA (siRNA) against claudin-3 treatment specifically decreased claudin-3 as seen by immunoblotting and immunofluorescent staining. Gastric TEER was significantly decreased with the treatment of siRNA against claudin-3. This is the first study to demonstrate that claudin-3 is involved in the barrier function of gastric epithelial cells and that rebamipide abolishes the H2O2-induced decrease in claudin-3 protein. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：154 / 157

页数：4

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