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J. Biol. Chem., Vol. 277, Issue 14, 12280-12287, April 5, 2002
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From the Departments of Recent experimental findings
involve corticotropin-releasing hormone (CRH) in the cellular response
to noxious stimuli and possibly apoptosis. The aim of the present work
was to examine the effect of CRH on apoptosis and the Fas/Fas ligand
system in an in vitro model, the PC12 rat pheochromocytoma
cell line, which is widely used in the study of apoptosis and at the
same time expresses the CRH/CRH receptor system. We have found the
following. CRH induced Fas ligand production and apoptosis. These
effects were mediated by the CRH type 1 receptor because its antagonist antalarmin blocked CRH-induced apoptosis and Fas ligand expression. CRH
activated p38 mitogen-activated protein kinase, which was found to be
essential for CRH-induced apoptosis and Fas ligand production. CRH also
promoted a rapid and transient activation of ERK1/2, which, however,
was not necessary for either CRH-induced apoptosis or Fas ligand
production. Thus, CRH promotes PC12 apoptosis via the CRH type 1 receptor, which induces Fas ligand production via activation of p38.
Corticotropin-releasing Hormone Induces Fas Ligand Production and
Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein
Kinase*
,,¶
Clinical
Chemistry-Biochemistry and § Pharmacology, School of
Medicine, University of Crete, Heraklion,
Crete GR-711 10, Greece
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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