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Molecular and Cellular Biology, June 1999, p. 4209-4218, Vol. 19, No. 6
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Protein Kinase Cdelta Mediates Neurogenic but Not Mitogenic Activation of Mitogen-Activated Protein Kinase in Neuronal Cells

Kevin C. Corbit,1 David A. Foster,2 and Marsha Rich Rosner1,*

Department of Pharmacological and Physiological Sciences and The Ben May Institute for Cancer Research, University of Chicago, Chicago, Illinois 60637,1 and Department of Biological Sciences, Hunter College of The City University of New York, New York, New York 100212

Received 27 October 1998/Returned for modification 11 January 1999/Accepted 22 March 1999

In several neuronal cell systems, fibroblast-derived growth factor (FGF) and nerve growth factor (NGF) act as neurogenic agents, whereas epidermal growth factor (EGF) acts as a mitogen. The mechanisms responsible for these different cellular fates are unclear. We report here that although FGF, NGF, and EGF all activate mitogen-activated protein (MAP) kinase (extracellular signal-related kinase [ERK]) in rat hippocampal (H19-7) and pheochromocytoma (PC12) cells, the activation of ERK by the neurogenic agents FGF and NGF is dependent upon protein kinase Cdelta (PKCdelta ), whereas ERK activation in response to the mitogenic EGF is independent of PKCdelta . Antisense PKCdelta oligonucleotides or the PKCdelta -specific inhibitor rottlerin inhibited FGF- and NGF-induced, but not EGF-induced, ERK activation. In contrast, EGF-induced ERK activation was inhibited by the phosphatidylinositol-3-kinase inhibitor wortmannin, which had no effect upon FGF-induced ERK activation. Rottlerin also inhibited the activation of MAP kinase kinase (MEK) in response to activated Raf, but had no effect upon c-Raf activity or ERK activation by activated MEK. These results indicate that PKCdelta functions either downstream from or in parallel with c-Raf, but upstream of MEK. Inhibition of PKCdelta also blocked neurite outgrowth induced by FGF and NGF in PC12 cells and by activated Raf in H19-7 cells, indicating a role for PKCdelta in the neurogenic effects of FGF, NGF, and Raf. Interestingly, the PKCdelta requirement is apparently cell type specific, since FGF-induced ERK activation was independent of PKCdelta in NIH 3T3 murine fibroblasts, in which FGF is a mitogen. These data demonstrate that PKCdelta contributes to growth factor specificity and response in neuronal cells and may also promote cell-type-specific differences in growth factor signaling.

* Corresponding author. Mailing address: Ben May Institute for Cancer Research, University of Chicago, 5481 S. Maryland Ave., MC 6027, Chicago, IL 60637-1470. Phone: (773) 702-0380. Fax: (773) 702-4634. E mail: mrosner{at}ben-may.bsd.uchicago.edu.

Molecular and Cellular Biology, June 1999, p. 4209-4218, Vol. 19, No. 6
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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