Hu B R, Wieloch T
Laboratory for Experimental Brain Research, Lund University Hospital, Sweden.
J Neurochem. 1994 Apr;62(4):1357-67. doi: 10.1046/j.1471-4159.1994.62041357.x.
Activation of trophic factor receptors stimulates tyrosine phosphorylation on proteins and supports neuronal survival. We report that in the recovery phase following reversible cerebral ischemia, tyrosine phosphorylation increases in the membrane fraction of the resistant hippocampal CA3/dentate gyrus (DG) region, whereas in the sensitive CA1 region or striatum, tyrosine phosphorylation is less marked or decreases. In the cytosolic fractions, a 42-kDa protein, identified as mitogen-activated protein (MAP) kinase, is markedly phosphorylated and activated immediately following ischemia, in particular in CA3/DG, but not in striatum. In the CA1 region, phosphorylation of MAP kinase is less intense and decreases later during reperfusion, which could explain the delay of neuronal degeneration in this structure. The data suggest that in ischemia-resistant neurons the growth factor receptor-coupled signaling cascade is stimulated and, through its effects on DNA transcription and mRNA translation, supports neuronal survival.
营养因子受体的激活可刺激蛋白质的酪氨酸磷酸化并支持神经元存活。我们报告，在可逆性脑缺血后的恢复阶段，抗缺血的海马CA3/齿状回（DG）区域的膜部分酪氨酸磷酸化增加，而在敏感的CA1区域或纹状体中，酪氨酸磷酸化不明显或减少。在胞质部分，一种被鉴定为丝裂原活化蛋白（MAP）激酶的42 kDa蛋白在缺血后立即被显著磷酸化并激活，特别是在CA3/DG区域，但在纹状体中则不然。在CA1区域，MAP激酶的磷酸化程度较低，且在再灌注后期下降，这可以解释该结构中神经元变性的延迟。数据表明，在抗缺血神经元中，生长因子受体偶联的信号级联被激活，并通过其对DNA转录和mRNA翻译的影响来支持神经元存活。
