Urocortin 1 and Urocortin 2 induce macrophage apoptosis via CRFR2

被引：78

作者：

Tsatsanis, C ^{[1
]}

Androulidaki, A

Dermitzaki, E

Charalampopoulos, I

Spiess, J

Gravanis, A

Margioris, AZ

机构：

[1] Univ Crete, Sch Med, Dept Clin Chem & Biochem, GR-71003 Iraklion, Crete, Greece

[2] Univ Crete, Sch Med, Dept Pharmacol, GR-71003 Iraklion, Crete, Greece

[3] Max Planck Inst Expt Med, Dept Mol Neuroendocrinol, D-37075 Gottingen, Germany

来源：

FEBS LETTERS | 2005年 / 579卷 / 20期

关键词：

macrophage; urocortin; CRFR2; apoptosis; bax;

D O I：

10.1016/j.febslet.2005.06.057

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：

Macrophages undergo apoptosis as a mechanism of regulating their activation and the inflammatory reaction. Macrophages express the Corticotropin-Releasing Factor Receptor-2 (CRFR2) the endogenous agonists of which, the urocortins, are also present at the site of inflammation. We have found that urocortins induced macrophage apoptosis in a dose- and time-dependent manner via CRFR2. In contrast to lipopolysaccharide (LPS)-induced apoptosis, the pro-apoptosis pathway activated by urocortins involved the pro-apoptotic Bax and Bad proteins and not nitric oxide, JNK and p38MAPK characteristic of LPS. In conclusion, our data suggest that endogenous CRFR2 ligands exert an anti-inflammatory effect via induction of macrophage apoptosis. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：4259 / 4264

页数：6

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