Time courses of increased expression of signaling transduction molecules induced by basic fibroblast growth factor in PC12 cells.
We previously demonstrated that basic fibroblast growth factor (bFGF) protected neuronal injury in in vivo experimental cerebral ischemia. The precise molecular mechanisms of the neuroprotective effect of bFGF, however, remains unsolved. We investigated time courses of up-regulated molecules involved in intracellular signaling transduction pathways induced by bFGF in PC12 cells to explore the possible neuroprotective mechanism of bFGF action. In Western blot analysis, bFGF increased expression of Ras mainly in the early stage up to 24h, returning to the baseline level at 48 h. Expression of phosphatidylinositol 3-kinase (PI 3-kinase) was enhanced throughout the early and later stages, and was more up-regulated at 48 h compared to 24 h. The present findings suggest that bFGF might promote cell survival or proliferation mainly via Ras, and PI 3-kinase might be involved in cell survival and differentiation in PC12 cells.
Kawamata
T
T
Department of Neurosurgery, Neurological Institute, Tokyo Women's Medical University, Japan. tkawamata@nij.twmu.ac.jp
Yamaguchi
T
T
Shin-ya
K
K
Hori
T
T
D000818:Animals; D015153:Blotting, Western; D002470:Cell Survival / Q000187:drug effects; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology*; D016716:PC12 Cells / Q000187:drug effects / Q000502:physiology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction / Q000502:physiology*; D013997:Time Factors; D020827:rap1 GTP-Binding Proteins / Q000378:metabolism*; D018631:ras Proteins / Q000378:metabolism*
D019253:Proto-Oncogene Proteins c-bcl-2; D016222:Fibroblast Growth Factor 2; D019869:Phosphatidylinositol 3-Kinases; D020827:rap1 GTP-Binding Proteins; D018631:ras Proteins