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PACAP Action in Nervous System Development, Regeneration, and Neuroblastoma Cell Proliferation
Author(s) -
WASCHEK JAMES A.,
DICICCOBLOOM EMANUEL M.,
LELIEVRE VINCENT,
ZHOU XINRONG,
HU ZHONGTING
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06959.x
Subject(s) - neurogenesis , axotomy , neural tube , endocrinology , medicine , microbiology and biotechnology , biology , neural development , pituitary adenylate cyclase activating peptide , regeneration (biology) , adenylate kinase , neuroblastoma , receptor , chemistry , neuropeptide , cell culture , embryo , vasoactive intestinal peptide , biochemistry , genetics , gene
A bstract : Pituitary adenylate cyclase activating peptide (PACAP) may play a role in neurogenesis, nerve injury, and neural tumor growth. A PACAP ligand receptor system functionally coupled to cAMP production was found to be expressed in the embryonic mouse neural tube at the onset of neurogenesis. PACAP was found to inhibit DNA synthesis and antagonize sonic hedgehog signaling in cells isolated from the neural tube, suggesting that PACAP interacts with patterning factors to regulate neurogenesis and phenotypic specification in the developing CNS. PACAP and PACAP receptor (PAC 1 ) mRNA levels were strongly increased and decreased, respectively, in motor neurons in adult rats after facial nerve axotomy, indicating that PACAP may also act in nerve regeneration. Experiments using a neuroblastoma tumor cell line model indicate that PACAP may execute growth‐related functions by activating MAP kinase in addition to cAMP‐dependent protein kinase A.