Abe K, Saito H
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, 113-0033, Tokyo, Japan.
Brain Res Dev Brain Res. 2000 Jul 30;122(1):81-5. doi: 10.1016/s0165-3806(00)00054-7.
Basic fibroblast growth factor (bFGF) has been reported to support the survival of brain neurons. In the present study, we investigated whether the neurotrophic effect of bFGF is mediated by the mitogen-activated protein kinase (MAPK) cascade in cultured rat cerebral cortical neurons. Recombinant human bFGF (0.1-10 ng/ml) induced phosphorylation of p44/42 MAPK (ERK1/2) in a concentration- and time-dependent manner. bFGF-induced ERK1/2 phosphorylation and promotion of neuronal survival were both blocked by U0126 and PD98059, inhibitors of the MAPK-activating enzyme MEK. These results suggest that the MEK/ERK signal transduction cascade is involved in the neurotrophic effect of bFGF.
据报道，碱性成纤维细胞生长因子（bFGF）可支持脑神经元的存活。在本研究中，我们调查了bFGF的神经营养作用是否由培养的大鼠大脑皮质神经元中的丝裂原活化蛋白激酶（MAPK）级联介导。重组人bFGF（0.1 - 10 ng/ml）以浓度和时间依赖性方式诱导p44/42 MAPK（ERK1/2）磷酸化。bFGF诱导的ERK1/2磷酸化和神经元存活促进均被MAPK激活酶MEK的抑制剂U0126和PD98059阻断。这些结果表明，MEK/ERK信号转导级联参与了bFGF的神经营养作用。
