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Originally published In Press as doi:10.1074/jbc.M909732199 on March 19, 2000
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J Biol Chem, Vol. 275, Issue 20, 15114-15121, May 19, 2000

Inhibition of NF-kappa B Activity and Enhancement of Apoptosis by the Neuropeptide Calcitonin Gene-related Peptide*

Isabelle MilletDagger §, Roderick J. Phillips||, Robert S. SherwinDagger , Sankar Ghosh||**Dagger Dagger , Reinhard E. Voll||, Richard A. Flavell||**§§, Agnès Vignery§, and Mercedes Rincón¶¶||||

From the Dagger  Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510, the ¶¶ Department of Medicine, Program of Immunobiology, University of Vermont, Burlington, Vermont 05405, the || Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, the ** Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510, and the § Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, Connecticut 06510

Calcitonin gene-related peptide (CGRP) is a neuropeptide produced by the central and peripheral nervous systems and by endocrine cells. CGRP exerts diverse biological effects on the cardiovascular, gastrointestinal, respiratory, central nervous and immune systems. Little is known, however, about the molecular mechanisms that mediate CGRP effects. Using the NFkappa B-luciferase reporter transgenic mice, here we show that CGRP selectively inhibits NF-kappa B-mediated transcription in thymocytes in vitro and in vivo. In contrast, CGRP does not affect transcription mediated by the AP-1 and NFAT transcription factors. CGRP inhibits the accumulation of NF-kappa B complexes in the nucleus by preventing phosphorylation and degradation of the NF-kappa B inhibitor Ikappa B. Inhibition of NF-kappa B activity is associated with the induction of apoptosis by CGRP in thymocytes. Together these results demonstrate for the first time the selective implication of the NF-kappa B signaling pathway in the regulatory function of the neuropeptide CGRP. Our study suggests a potential molecular mechanism by which CGRP can induce cell death in thymocytes.

* This work was supported in part by National Institutes of Health Grants AI42138 (to M. R.) and AR41965 and AR41942 (to A.V).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.

Recipient of a Juvenile Diabetes Foundation fellowship.

Dagger Dagger Associated investigator of the Howard Hughes Medical Institute.

§§ Investigator of the Howard Hughes Medical Institute.

|||| To whom correspondence should be addressed: Dept. of Medicine/Immunobiology Program, Given Medical Building C305, University of Vermont, Burlington, VT 05405. Tel.: 802-656-0937; Fax: 802-656-3854.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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