IGF-I promotes Schwann cell motility and survival via activation of Akt

被引:54
作者
Cheng, HL
Steinway, M
Delaney, CL
Franke, TF
Feldman, EL
机构
[1] Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA
[2] Columbia Univ, Dept Pharmacol, New York, NY 10032 USA
关键词
IGF-I; Schwann cell; Akt; motility; apoptosis;
D O I
10.1016/S0303-7207(00)00324-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
We previously reported insulin-like growth factor-I (IGF I) promotes Schwann cell (SC) motility and rescues SC from apoptosis induced by serum deprivation. This effect is mediated by phosphatidylinositol-3 (PI-3) kinase. In the current study, we examined the role of Akt, a downstream kinase of PI-3K, in SC motility and IGF I mediated protection from apoptosis. IGF-I induces Akt phosphorylation at Ser473, an event which may be blocked by pretreatment with a PI-3K inhibitor, LY294002. In dominant negative K179M Akt (K179M) transfected SC, however, Akt is not activated in response to IGF-I. In addition, ICF-I is unable to promote SC motility and survival in K179M SC. These results suggest a critical role for Akt in IGF-I mediated motility and survival in SC. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:211 / 215
页数:5
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