Nitric oxide mediates membrane depolarization-promoted survival of rat neuronal PC12 cells

被引：12

作者：

Kim, TW ^{[1
]}

Lee, CH ^{[1
]}

Choi, CY ^{[1
]}

Kwon, NS ^{[1
]}

Baek, KJ ^{[1
]}

Kim, YG ^{[1
]}

Yun, HY ^{[1
]}

机构：

[1] Chung Ang Univ, Coll Med, Dept Biochem, Dongjak Ku, Seoul 156756, South Korea

来源：

NEUROSCIENCE LETTERS | 2003年 / 344卷 / 03期

关键词：

nitric oxide; pheochromocytoma-12; cells; survival; membrane depolarization; potassium chloride; Ras; cGMP;

D O I：

10.1016/S0304-3940(03)00451-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Membrane depolarization promotes neuronal survival through increases in intracellular calcium. Nitric oxide (NO) is a signaling molecule involved in many neuronal activity-dependent events. Since neuronal NO is generated by NO synthase (NOS) in a calcium-dependent manner and was shown to promote cell survival, we tested whether NO is involved in depolarization-promoted survival in neuronally differentiated PC12 cells. NOS inhibitor attenuated depolarization-promoted survival and NO donors promoted survival. This effect was partially cGMP-dependent as a guanylyl cyclase inhibitor decreased NO-promoted survival. Ras inhibitor, Erk blocker or phosphatidylinositol 3-kinase inhibitor decreased depolarization- or NO donor-promoted survival. Depolarization-induced Ras activation was blocked by NOS inhibitor. Inducible expression of dominant negative Ras or S-nitrosylation-defective Ras attenuated depolarization- or NO donor-promoted survival. Thus, NO might be a mediator via Ras and cGMP pathways in depolarization-promoted survival in neuronal PC12 cells. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：209 / 211

页数：3

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