期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 22, 期 4, 页码 487-500出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S1044-7431(02)00042-8
关键词
-
Recently. we have demonstrated that tumor necrosis factor-alpha (TNF-alpha) rescues retinal ganglion cells (RGCs) from retrograde cell death in vivo after axotomy of the optic nerve. The mechanism of RGC rescue was dependent on TNF-receptor I-mediated potassium current reduction and consecutive activation of the phosphatidylinositol 3-kinase (PI3-K)/Akt pathway. Here, we present evidence that interleukin-1beta (IL-1beta) also promotes RGC survival, but shows distinct differences with respect to its neuroprotective mechanisms. Using whole-cell and outside-out patch-clamp techniques, we observed that IL-1beta decreased both inward sodium current amplitudes and outward potassium current amplitudes. Counteracting these effects by sodium or potassium channel opening inhibited the survival-promoting effects of this cytokine. IL-1beta-induced current reduction could not be abolished by the interleukin-1 receptor antagonist, indicating that the electrophysiological effects of IL-1beta are independent of interleukin-1 receptor I (IL-1RI) activation. Western blot analysis revealed an IL-1beta-induced IL-1RI-dependent Upregulation of phospho-Akt. Antagonism of the survival-promoting effects of IL-1beta by PI3-K inhibition revealed the functional relevance of the PI3-K/Akt pathway in IL-1beta-induced signal transduction in vivo. (C) 2003 Elsevier Science (USA). All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据