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Urocortin 1 and Urocortin 2 induce macrophage apoptosis via CRFR 2
Author(s) -
Tsatsanis Christos,
Androulidaki Ariadne,
Dermitzaki Erini,
Charalampopoulos Ioannis,
Spiess Joachim,
Gravanis Achille,
Margioris Andrew N.
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.06.057
Subject(s) - apoptosis , urocortin , lipopolysaccharide , macrophage , endogeny , inflammation , nitric oxide , microbiology and biotechnology , chemistry , receptor , biology , immunology , biochemistry , endocrinology , in vitro
Macrophages undergo apoptosis as a mechanism of regulating their activation and the inflammatory reaction. Macrophages express the Corticotropin‐Releasing Factor Receptor‐2 (CRFR 2 ) 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 CRFR 2 . 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 CRFR 2 ligands exert an anti‐inflammatory effect via induction of macrophage apoptosis.