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   <subfield code="a">Induction of TNF-α by LPS in Schwann Cell is Regulated by MAPK Activation Signals</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Chun Cheng, Yongwei Qin, Xiaoyi Shao, Haibo Wang, Yongjing Gao, Mengling Cheng, Aiguo Shen]</subfield>
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   <subfield code="a">Mitogen-activated protein kinases (MAPKs) are important mediators of cytokine expression and are critically involved in the immune response. The lipopolysaccharide (LPS) of gram-negative bacteria induces the expression of cytokines and proinflammatory genes via the toll-like receptor 4 (TLR4) signaling pathway in diverse cell types. Invivo, Schwann cells (SCs) at the site of injury may also produce tumor necrosis factor-- α (TNF-α). However, the precise mechanisms of TNF-α synthesis are still not clear. The purpose of the present study was to elucidate the underlying molecular mechanisms in the cultured SCs for its ability to activate the MAPKs and TNF-α gene, in response to LPS. Using enzyme-linked immunosorbent assay (ELISA), it was confirmed that treatment with LPS stimulated the synthesis of TNF-α in a concentration- and time-dependent manner. Intracellular location of TNF-α was detected under confocal microscope. Moreover, LPS activated extracellular signal-regulated kinase (ERK1/2), P38 and stress activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) and induced their phosphorylation. LPS-elicited SCs TNF-α production was also drastically suppressed by PD98059 (ERK inhibitor), SB202190 (P38 inhibitor), or SP600125 (SAPK/JNK inhibitor). Additionally, the expression of CD14 and TLR4 was examined by RT-PCR. It was demonstrated that the expression of CD14, TLR4 was crucial for the SCs responses to LPS. In conclusion, the results provide novel mechanisms for the response of SCs to LPS stimulation, through MAPKs signaling pathways.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2007</subfield>
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   <subfield code="a">Lipopolysaccharide</subfield>
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   <subfield code="a">Cheng</subfield>
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   <subfield code="u">Key Laboratory for Neuroregeneration of JiangSu Province, Nantong University, 19 Qixiu Road, 226001, Nantong, Jiangsu, PR China</subfield>
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   <subfield code="u">Department of Parasitology, Medical College, Nantong University, Nantong, PR China</subfield>
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   <subfield code="a">Shao</subfield>
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   <subfield code="u">Department of Microbiology and Immunology, Medical College, Nantong University, Nantong, PR China</subfield>
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   <subfield code="a">Wang</subfield>
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   <subfield code="u">Department of Microbiology and Immunology, Medical College, Nantong University, Nantong, PR China</subfield>
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   <subfield code="u">Institute of Nautical Medicine, Nantong University, Nantong, PR China</subfield>
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   <subfield code="u">Key Laboratory for Neuroregeneration of JiangSu Province, Nantong University, 19 Qixiu Road, 226001, Nantong, Jiangsu, PR China</subfield>
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   <subfield code="t">Cellular and Molecular Neurobiology</subfield>
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