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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Cytokine and intracellular signaling regulation of tissue factor expression in astrocytes.
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Cytokine and intracellular signaling regulation of tissue factor expression in astrocytes.

机译：细胞因子和星形细胞中细胞因子对组织因子表达的调控。

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There is evidence that inflammatory cytokines such as IL-1beta, TNFalpha, and IL-6 are involved in the pathogenesis of cerebrovascular disorders including stroke. One action of cytokines that contributes to diseases in peripheral tissues is upregulation of the procoagulant receptor tissue factor (TF). In the CNS, astrocytes are the primary cells that express TF; although little is known about how TF is regulated in these cells. Experiments were performed to evaluate the effect of cytokine treatment on TF activity in primary cultures of murine cortical astrocytes and in the human astrocytoma cell line (CCF). IL-1beta treatment induced a 2.5-fold increase in TF activity in the primary astrocytes and a 3-fold induction in the astrocytoma cells. TNFalpha treatment induced a 2.5-fold increase in TF activity in both the primary astrocytes and astrocytoma cells. IL-6 upregulated TF activity 2-fold in primary astrocytes, however, it had no effect on TF activity in the astrocytoma cells. The signaling pathways regulating TF expression in these cells were examined by using staurosporine, a broad spectrum inhibitor of serine-threonine protein kinases, and by examining the effects of intermediates in the sphingomyelin signaling pathway. Staurosporine inhibited IL-1beta-induced TF activity in the primary astrocytes but did not effect IL-1beta- or TNFalpha-induced TF activity in the astrocytoma cells. TF activity in the astrocytoma cells was upregulated 1.5-fold over constitutive levels by a ceramide analogue or the enzyme sphingomyelinase, however the ceramide analogue had no effect on TF activity in the primary astrocytes. These results suggest inflammatory cytokines can upregulate TF activity in astrocytes and the astrocytoma CCF cell line although the two cell types appear to utilize different signaling pathways to mediate TF expression. Further studies will be important to more completely define the signaling regulation of TF in astrocytes since alterations in brain TF levels may play a key role in CNS pathophysiology.
机译：有证据表明，炎症性细胞因子（例如IL-1beta，TNFalpha和IL-6）与脑血管疾病（包括中风）的发病机理有关。导致周围组织疾病的细胞因子的一种作用是促凝受体组织因子（TF）的上调。在中枢神经系统中，星形胶质细胞是表达TF的原代细胞。尽管对这些细胞中TF的调控机制知之甚少。进行实验以评估细胞因子处理对鼠皮质星形胶质细胞原代培养物和人星形细胞瘤细胞系（CCF）中TF活性的影响。 IL-1β处理在原代星形胶质细胞中诱导TF活性增加2.5倍，在星形细胞瘤细胞中诱导3倍的诱导。 TNFalpha处理在原代星形胶质细胞和星形细胞瘤细胞中诱导TF活性增加了2.5倍。 IL-6上调星形胶质细胞的TF活性2倍，但是，它对星形细胞瘤细胞的TF活性没有影响。通过使用星形孢菌素（一种丝氨酸-苏氨酸蛋白激酶的广谱抑制剂），并通过检查鞘磷脂信号通路中的中间体的作用，可以检查调节这些细胞中TF表达的信号通路。星形孢菌素抑制星形胶质细胞中IL-1β诱导的TF活性，但不影响星形细胞瘤细胞中IL-1β或TNFalpha诱导的TF活性。神经酰胺类似物或鞘磷脂酶将星形细胞瘤细胞中的TF活性上调至本构水平的1.5倍，但是神经酰胺类似物对原代星形胶质细胞的TF活性没有影响。这些结果表明，炎性细胞因子可以上调星形胶质细胞和星形细胞瘤CCF细胞系中的TF活性，尽管这两种细胞类型似乎利用不同的信号传导途径来介导TF表达。进一步的研究对于更完整地定义星形胶质细胞中TF的信号传导调节至关重要，因为脑TF水平的改变可能在中枢神经系统病理生理中起关键作用。

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