Regulation of nuclear factor-κB in intestinal epithelial cells in a cell model of inflammation

被引：24

作者：

Homaidan, FR ^{[1
]}

Chakroun, I

El-Sabban, ME

机构：

[1] Amer Univ Beirut, Fac Med, Dept Physiol, Beirut, Lebanon

[2] Amer Univ Beirut, Fac Med, Dept Human Morphol, Beirut, Lebanon

来源：

MEDIATORS OF INFLAMMATION | 2003年 / 12卷 / 05期

关键词：

nuclear factor-kappa B; interleukin-1; inflammatory bowel disease; inflammation; intestinal epithelial cells; PROTEASOME INHIBITOR PS-341; PHASE-I TRIAL; HEMATOLOGIC MALIGNANCIES; TRANSCRIPTION FACTOR; ALPHA PROTEOLYSIS; PHOSPHORYLATION; ACTIVATION; APOPTOSIS; CERAMIDE; PROTEINS;

D O I：

10.1080/09629350310001619681

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

BACKGROUND: Interleukin-1 (IL-1), an inflammatory cytokine whose levels are elevated in inflamed mucosa, causes part of its effect on intestinal epithelial cells (IEC) through inducing ceramide production. Aim: To study the role of nuclear factor-kappaB (NF-kappaB), a pro-inflammatory and anti-apoptotic factor, in IL-1-treated IEC. Methods: NF-kappaB activity and levels of apoptotic proteins were assessed by electrophoretic mobility shift assay and RNA-protection assay, respectively. Results: IL-1 and ceramide, which have been shown to partially mediate IL-l effects on IEC, activated NF-kappaB levels significantly. This activation was due to a decrease in IkappaB-alpha and IkappaB-beta protein levels. Moreover, the ratio of mRNA levels of anti-apoptotic to proapoptotic proteins was significantly increased in IL-1-treated IEC. Conclusion: NF-kappaB may play a key role in the regulation of the expression of pro-inflammatory and/or apoptotic genes in inflammatory bowel disease, making this protein an attractive target for therapeutic intervention.

引用

页码：277 / 283

页数：7

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