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J Biol Chem, Vol. 274, Issue 42, 29666-29671, October 15, 1999
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From the We recently showed that mouse semaphorin H (MSH),
a secreted semaphorin molecule, acts as a chemorepulsive factor on
sensory neurites. In this study, we found for the first time that MSH induces neurite outgrowth in PC12 cells in a dose-dependent
manner. Comparison of Ras-mitogen-activated protein kinase (MAPK)
signaling pathways between MSH and nerve growth factor (NGF) revealed
that these pathways are crucial for MSH action as well as NGF. K-252a, an inhibitor of tyrosine autophosphorylation of tyrosine kinase receptors (Trks), did not inhibit the action of MSH, suggesting that
MSH action occurs via a different receptor than NGF. L- and N-types of
voltage-dependent Ca2+ channel blockers,
diltiazem and Group of Neurobiology, School of Allied
Health Sciences, Osaka University Faculty of Medicine, Yamadaoka 1-7, Suita-shi, Osaka, 565-0871, Japan, the § First Department of
Oral and Maxillo-Facial Surgery, Osaka University Faculty of Dentistry,
Yamadaoka 1-8, Suita-shi, Osaka, 565-0871, Japan, the ¶ Department
of Molecular Genetic Research, National Institute for Longevity
Sciences, Morioka-cho, Ohbu-shi, 474-5822, Japan, and the
Division of Biochemistry and Cellular Biology, National
Institute of Neuroscience, National Center of Neurology and Psychiatry,
4-1-1 Kodaira, Tokyo 187-8502, Japan
-conotoxin, inhibited MSH-induced neurite outgrowth
and MAPK phosphorylation in a Ca2+-dependent
manner. A transient elevation in intracellular Ca2+ level
was observed upon MSH stimulation. These findings suggest that
extracellular Ca2+ influx, followed by activation of the
Ras-MAPK signaling pathway, is required for MSH induced PC12 cell
neurite outgrowth.
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