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) prote cted neuronal injury in in vivo experimental cerebral ischemia. The precise molecular mechanisms of the neuroprotective effect of bFGF, however, remai ns unsolved. We investigated time courses of up-regulated molecules involve d 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 Pas mainly in the early stage up to 24h, returning to the baseline level at 48h. Expression of pho sphatidylinositol 3-kinase (PI 3-kinase) was enhanced throughout the early and later stages, and was more up-regulated at 48h compared to 24h. The pre sent findings suggest that bFGF might promote cell survival or proliferatio n mainly via Pas, and PI 3-kinase might be involved in cell survival and di fferentiation in PC12 cells.