SSeCKS 通过激活施万细胞中的 p38 和 JNK 通路促进肿瘤坏死因子-α自分泌。
SSeCKS promotes tumor necrosis factor-alpha autocrine via activating p38 and JNK pathways in Schwann cells.
机构信息
Department of Osteology, Affiliated Jiangyin Hospital of Nantong University, and The Jiangsu Province Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, Jiangsu, People's Republic of China.
出版信息
Cell Mol Neurobiol. 2010 Jul;30(5):701-7. doi: 10.1007/s10571-009-9494-z. Epub 2010 Jan 29.
Abstract
Tumor necrosis factor-alpha (TNF-alpha) derived from activated Schwann cells (SCs) plays a critical role as an inflammatory mediator in the peripheral nervous system disease. TNF-alpha could act as an autocrine mediator in SC activation. In this study, we found knockdown Src-suppressed protein kinase C substrate (SSeCKS) expression suppressed TNF-alpha production induced by TNF-alpha, overexpression of SSeCKS could promoted TNF-alpha autocrine in SCs. Such effects might be resulted in SSeCKS promoted p38 and JNK activation in SCs treated by TNF-alpha. Thus present data show that while SCs activation, SSeCKS may plays an important role in the release of inflammatory mediators.
摘要
肿瘤坏死因子-α（TNF-α）来源于激活的雪旺细胞（SCs），在周围神经系统疾病中作为炎症介质发挥着关键作用。TNF-α可作为SCs激活的自分泌介质。在这项研究中，我们发现Src 抑制蛋白激酶 C 底物（SSeCKS）的敲低表达抑制了 TNF-α诱导的 TNF-α产生，SSeCKS 的过表达可促进 SCs 中 TNF-α的自分泌。这些效应可能是由于 SSeCKS 促进了 TNF-α处理后的 SCs 中 p38 和 JNK 的激活。因此，目前的数据表明，在SCs 激活时，SSeCKS 可能在炎症介质的释放中发挥重要作用。
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