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Updated: Jun 16, 2026

Analyzing Murine Schwann Cell Development Along Growing Axons
Published on: November 21, 2012
SSeCKS promotes tumor necrosis factor-alpha autocrine via activating p38 and JNK pathways in Schwann cells
Zhengming Zhou1, Tao Tao, Yuhong Ji
1Department 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.
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.
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