Induction of IκB:: atrial natriuretic peptide as a regulator of the NF-κB pathway

被引：54

作者：

Kiemer, AK ^{[1
]}

Weber, NC ^{[1
]}

Vollmar, AM ^{[1
]}

机构：

[1] Univ Munich, Ctr Drug Res, Dept Pharm, D-81377 Munich, Germany

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2002年 / 295卷 / 05期

关键词：

cardiovascular hormone; natriuretic peptides; cGMP; NPR-A; adhesion molecules; TNF-alpha; endothelial cells; HUVEC;

D O I：

10.1016/S0006-291X(02)00807-0

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：

Atrial natriuretic peptide (ANP) was shown to possess anti-inflammatory potential due to its potency to inhibit the production of inflammatory mediators, such as TNF-alpha. The aim of this study was to determine potential effects of ANP on endothelial cells targeted by TNF-alpha. HUVEC were treated with TNF-alpha and expression of adhesion molecules was investigated by FACS and RTPCR. Pre-treatment of cells with ANP (30 min) significantly reduced TNF-alpha-induced cell surface protein and mRNA expression of E-selectin and ICAM-1, whereas it did not influence VCAM-1. ANP reduced TNF-alpha-induced NF-kappaB activity, which was paralleled by a decreased translocation of p65 to nuclei. ANP did not alter TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, but attenuated degradation of IkappaB-epsilon. Moreover, ANP leads to a transcriptional induction of IkappaB-alpha. The induction of IkappaB by ANP is suggested as a novel mechanism for regulating inflammatory signalling in endothelial cells, leading to reduced TNF-alpha-induced expression of adhesion molecules. (C) 2002 Elsevier Science (USA). All rights reserved.

引用

页码：1068 / 1076

页数：9

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