Heat shock induces neurite outgrowth in PC12m3 cells via the p38 mitogen-activated protein kinase pathway
Heat shock induces neurite outgrowth in PC12m3 cells via the p38 mitogen-activated protein kinase pathway
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DOI：
10.1016/j.brainres.2004.07.053
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发表时间：
2004-11-12
期刊：
影响因子：
2.9
通讯作者：
Furuta, T
中科院分区：
文献类型：
--
作者：
Kano, Y;Nakagiri, S;Furuta, T
我们研究了p38丝裂原活化蛋白激酶（MAPK）途径在热休克诱导的PC12突变细胞神经突起生长中的作用，其中神经生长因子（NGF）诱导的神经突起生长受损。当培养的PC12突变体（PC12m3）细胞暴露于44 ℃热应激10分钟时，p38 MAPK活性增加，神经突生长大大增强。p38 MAPK抑制剂BS 203580可抑制神经突起的生长。PC12m3细胞的长期热处理引起细胞死亡，这是由SB203580增强。这些结果表明，热诱导的p38 MAPK的激活是负责的突起生长和存活的PC 12 m3细胞。(C)2004 Elsevier B.V.保留所有权利。
We investigated the role of the p38 mitogen-activated protein kinase (MAPK) pathway in heat-shock-induced neurite outgrowth of PC12 mutant cells in which nerve growth factor (NGF)-induced neurite outgrowth is impaired. When cultures of the PC12 mutant (PC12m3) cells were exposed to heat stress at 44 degreesC for 10 min, activity of p38 MAPK increased and neurite outgrowth was greatly enhanced. The neurite extension was inhibited by the p38 MAPK inhibitor BS203580. Longer heat treatment of PC12m3 cells provoked cell death, which was enhanced by SB203580. These findings suggest that heat-induced activation of p38 MAPK is responsible for the neurite outgrowth and survival of PC12m3 cells. (C) 2004 Elsevier B.V. All rights reserved.