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首页> 外文期刊>Cytokine >Oncostatin M activates stat DNA binding and transcriptional activity in primary human fetal astrocytes: low- and high-passage cells have distinct patterns of stat activation.
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Oncostatin M activates stat DNA binding and transcriptional activity in primary human fetal astrocytes: low- and high-passage cells have distinct patterns of stat activation.

机译：抑癌素M激活人类胎儿星形胶质细胞中的stat DNA结合和转录活性：低和高传代细胞具有不同的stat激活模式。

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摘要

In this study we explored the activation of the JAK/Stat pathway by gp 130 family cytokines in primary human astrocytes. We report that of four gp 130 cytokines tested, only oncostatin M (OnM) resulted in the activation of Stat molecules. To test that the induced molecules were transcriptionally active, transcription from a Stat-responsive reporter plasmid (from the acute-phase gene alpha-2 macroglobulin) transiently transfected into astrocytes was assessed after activation by OnM and was blocked by cotransfection with dominant-negative Stat3 encoding plasmids strongly suggesting that the activation was Stat-mediated. While DNA binding complexes comprised of both Stat1 and Stat3 were induced in low-passage cells, only those containing Stat3 were formed by extracts from high-passage cells. Stat1 protein was detected in the cytoplasm of high-passage cells indicating that the inability to form SIF-B and -C complexes was due to a lack of activation of Stat1 rather than a lack of expression. These results indicate a fundamental difference between low- and high-passage astrocytes in response to cytokine treatment that might result in distinct patterns of gene expression through altered ratios of activated Stat3 and Stat1. Copyright 2000 Academic Press.
机译：在这项研究中，我们探索了人类原代星形胶质细胞中gp 130家族细胞因子对JAK / Stat途径的激活。我们报告说，在测试的四种gp 130细胞因子中，只有抑癌素M（OnM）导致Stat分子的激活。为了测试诱导的分子是否具有转录活性，在通过OnM激活后评估了瞬时转染到星形胶质细胞中的Stat反应性报告基因质粒（来自急性期基因alpha-2巨球蛋白）的转录，并通过与显性阴性Stat3共转染而被阻断编码质粒强烈提示激活是Stat介导的。虽然在低代细胞中诱导了同时包含Stat1和Stat3的DNA结合复合物，但仅通过高代细胞的提取物形成了包含Stat3的复合物。在高传代细胞的细胞质中检测到Stat1蛋白，这表明无法形成SIF-B和-C复合体是由于Stat1的激活而不是表达的缺乏。这些结果表明，低通量和高通量星形胶质细胞对细胞因子治疗的根本区别可能是通过改变激活的Stat3和Stat1的比例导致基因表达的不同模式。版权所有2000学术出版社。

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