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Vol. 54, Issue 3, 547-558, September 1998
Department of Pharmacology, School of Pharmacy, Faculty of
Medicine, The Hebrew University of Jerusalem, Jerusalem 91010, Israel
(P.L.),
Section on Growth Factors, The 38-amino-acid isoform of pituitary adenylate cyclase-activating
polypeptide (PACAP38) elicits a robust outgrowth of neurites in
cultured PC12 cells. Initiation of neurite outgrowth occurs within 4-8
hr after the addition of PACAP38. Treatment with PACAP38 does not
elicit collateral activation of p140trk nerve growth factor
receptor tyrosine kinase activity, nor is it associated with tyrosine
phosphorylation of suc1-associated neurotrophic factor target, a
selective target of neurotrophin tyrosine kinase receptors.
Coadministration of epidermal growth factor with PACAP38 elicits an
enhanced response. Induction of neurites is also observed on the
addition of PACAP38 to dominant negative Src and Ras PC12 cell
variants. PACAP38 stimulates extracellular signal-regulated kinase
(Erk) activity >10-fold within 5 min, and the effect is augmented by
cotreatment with epidermal growth factor. Pretreatment with the
cAMP-dependent protein kinase-selective inhibitor, H-89, is ineffective
as an antagonist of PACAP38-induced neurite outgrowth, whereas
down-regulation of protein kinase C (PKC) by phorbol ester or
incubation with PKC-selective inhibitors GF109203X and calphostin C
effectively blocks PACAP38-stimulated neurite formation. Stimulation of
Erk activity is inhibited by incubation with PD90859, a pharmacological
antagonist of the threonine/tyrosine dual-specificity Erk.
Inhibition of ligand-stimulated Erk activation prevents PACAP38-induced
neurite outgrowth. Collectively, these findings indicate that
PACAP38-stimulated neuritogenesis requires PKC and Erk activation but
is independent of cAMP-dependent protein kinase, nerve growth factor
receptor tyrosine kinase, p21ras G protein, and
pp60c-src cytoplasmic tyrosine kinase.
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics
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