Crosstalk between p38, Hsp25 and Akt in spinal motor neurons after sciatic nerve injury

被引:79
作者
Murashov, AK [1 ]
Haq, IU
Hill, C
Park, E
Smith, M
Wang, X
Wang, XY
Goldberg, DJ
Wolgemuth, DJ
机构
[1] E Carolina Univ, Brody Sch Med, Dept Physiol, Greenville, NC 27858 USA
[2] Columbia Univ Coll Phys & Surg, Dept Obstet & Gynecol, Ctr Reprod Sci, New York, NY 10032 USA
[3] Columbia Univ Coll Phys & Surg, Dept Pharmacol, New York, NY 10032 USA
[4] Columbia Univ Coll Phys & Surg, Ctr Neurobiol & Behav, New York, NY 10032 USA
[5] Columbia Univ Coll Phys & Surg, Dept Genet & Dev, New York, NY 10032 USA
来源
MOLECULAR BRAIN RESEARCH | 2001年 / 93卷 / 02期
基金
美国国家航空航天局;
关键词
hsp25; p38; Akt; regeneration; spinal cord; motor neuron;
D O I
10.1016/S0169-328X(01)00212-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The p38 stress-activated protein kinase pathway is involved in regulation of phosphorylation of Hsp25, which in turn regulates actin filament dynamic in non-neuronal cells. We report that p38, Hsp25 and Akt signaling pathways were specifically activated in spinal motor neurons after sciatic nerve axotomy. The activation of the p38 kinase was required for induction of Hsp25 expression. Furthermore, Hsp25 formed a complex with Akt, a member of PI-3 kinase pathway that prevents neuronal cell death. Together, our observations implicate Hsp25 as a central player in a complex system of signaling that may both promote regeneration of nerve fibers and prevent neuronal cell death in the injured spinal cord. (C) 2001 Elsevier Science B V All rights reserved.
引用
收藏
页码:199 / 208
页数:10
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