Calcitonin gene-related peptide induces AP-1 activity by a PKA and c- fos-dependent mechanism in pre-B cells

Calcitonin gene-related peptide (CGRP) is a sensory neuropeptide with regulatory influences on immune and inflammatory responses and early B lymphocyte differentiation. Little is known about its cellular mechanisms. These studies examined whether CGRP induces c- fos. CGRP induced a transient concent...

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Bibliographic Details
Published in:Journal of neuroimmunology 2002-02, Vol.123 (1), p.83-90
Main Authors: McGillis, Joseph P, Miller, Christopher N, Schneider, David B, Fernandez, Stefan, Knopf, Melissa
Format: Article
Language:English
Subjects:
Animals
AP-1
B cell differentiation
B lymphocyte
B-Lymphocytes - metabolism
Bone marrow
Bone Marrow - metabolism
c- fos
Calcitonin Gene-Related Peptide - pharmacology
CGRP
Cyclic AMP-Dependent Protein Kinases - physiology
Enzyme Activation
Hematopoietic Stem Cells - metabolism
Male
Mice
Mice, Inbred BALB C
Proto-Oncogene Proteins c-fos - genetics
Proto-Oncogene Proteins c-fos - physiology
Transcription Factor AP-1 - metabolism
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Summary:Calcitonin gene-related peptide (CGRP) is a sensory neuropeptide with regulatory influences on immune and inflammatory responses and early B lymphocyte differentiation. Little is known about its cellular mechanisms. These studies examined whether CGRP induces c- fos. CGRP induced a transient concentration-dependent increase in c- fos in a CGRP receptor expressing pre-B cell line, 70Z/3. CGRP did not induce c- jun, jun B or jun D. A protein kinase A (PKA) inhibitor blocked c- fos induction by CGRP, suggesting that the mechanism depends on cAMP induction of PKA. CGRP induced AP-1 binding activity in the nucleus, indicating that CGRP regulates expression of specific target genes. CGRP also induced c- fos in B220 + enriched cells from bone marrow. These results suggest that regulatory influences of CGRP on early B cells and in other tissues can involve a cAMP/PKA, c- fos/AP-1-dependent pathway for regulation of specific genes.
ISSN:0165-5728
1872-8421
DOI:10.1016/S0165-5728(01)00484-2