Src 抑制性 C 激酶底物调节大鼠星形胶质细胞中脂多糖诱导的肿瘤坏死因子-α 生物合成。
Src suppressed C kinase substrate regulates the lipopolysaccharide-induced TNF-alpha biosynthesis in rat astrocytes.
作者信息
Sun Lin-lin, Cheng Chun, Liu Hai-ou, Shen Cong-cong, Xiao Feng, Qin Jing, Yang Jun-ling, Shen Ai-guo
机构信息
Department of Immunology and Microbiology, Medical College of Nantong University, Nantong 226001, People's Republic of China.
出版信息
J Mol Neurosci. 2007;32(1):16-24. doi: 10.1007/s12031-007-0003-x.
The protein kinase C (PKC) is known to be a critical component in the signaling cascades that lead to astrocyte-activation. To further understand the mechanism of PKC signaling in astrocyte-activation, we investigated the effect of SSeCKS, a PKC substrate, on LPS-induced cytokine expression in astrocytes by RT-PCR and enzyme-linked immunosorbent assay. Exposure of the cells to LPS induced rapid translocation of SSeCKS to the perinuclear sides, ERK activation and pronounced TNF-alpha production, which can be inhibited by the PKC inhibitor Gö6983. By using siRNA knockdown of SSeCKS expression, LPS-induced signaling events were partly inhibited, including ERK activation, inducible TNF-alpha biosynthesis and secretion. These results suggest that SSeCKS is involved in the LPS-induced TNF-alpha expression in astrocytes mediated by PKC.
蛋白激酶C（PKC）是导致星形胶质细胞激活的信号级联反应中的关键组成部分。为了进一步了解PKC信号在星形胶质细胞激活中的机制，我们通过逆转录聚合酶链反应（RT-PCR）和酶联免疫吸附测定，研究了PKC底物富含半胱氨酸的酸性分泌蛋白（SSeCKS）对脂多糖（LPS）诱导的星形胶质细胞细胞因子表达的影响。细胞暴露于LPS会诱导SSeCKS迅速转位至核周区域、细胞外调节蛋白激酶（ERK）激活以及显著的肿瘤坏死因子-α（TNF-α）产生，而这可被PKC抑制剂Gö6983抑制。通过使用小干扰RNA（siRNA）敲低SSeCKS表达，LPS诱导的信号事件包括ERK激活、诱导型TNF-α生物合成和分泌均受到部分抑制。这些结果表明，SSeCKS参与了PKC介导的LPS诱导的星形胶质细胞TNF-α表达。
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