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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 >Enhanced phosphatidylinositol 4-phosphate 5-kinase alpha expression and PI(4,5)P2 production in LPS-stimulated microglia.
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Enhanced phosphatidylinositol 4-phosphate 5-kinase alpha expression and PI(4,5)P2 production in LPS-stimulated microglia.

机译：在LPS刺激的小胶质细胞中增强磷脂酰肌醇4-磷酸5激酶α表达和PI（4,5）P2的产生。

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摘要

Microglia are the major glial cells responsible for immune responses against harmful substances in the central nervous system. Type I phosphatidylinositol 4-phosphate 5-kinase alpha (PIP5Kalpha) and its lipid product, phosphatidylinositol 4,5-bisphosphate (PI[4,5]P(2)), regulate important cell surface functions. Here, we report that lipopolysaccharide (LPS) significantly enhanced PIP5Kalpha mRNA and protein expression levels in a time- and concentration-dependent manner in microglia. Furthermore, LPS stimulation led to a robust increase in PI(4,5)P(2) in the plasma membrane, demonstrated by PI(4,5)P(2) immunostaining or PI(4,5)P(2) imaging using a PI(4,5)P(2)-specific probe, tubby (R332H), fused to yellow fluorescent protein. Phosphatidylinositol 3-kinase, p38 mitogen-activated protein kinase (MAPK), p42/44 MAPK, and c-Jun N-terminal kinase signaling pathway inhibitors clearly reduced PIP5Kalpha expression, indicating that these pathways are necessary for LPS-induced PIP5Kalpha expression. In addition, inhibition of nuclear factor-kappaB and Sp1 transcription factors interfered with the LPS-induced upregulation of PIP5Kalpha. Delivery of PI(4,5)P(2) into microglia increased the expression of interleukin-1beta and tumor necrosis factor alpha. These findings indicate that PIP5Kalpha upregulation and the subsequent rise in PI(4,5)P(2) in LPS-stimulated microglia may positively regulate microglial inflammatory responses.
机译：小胶质细胞是负责针对中枢神经系统中有害物质的免疫反应的主要神经胶质细胞。 I型磷脂酰肌醇4-磷酸5激酶α（PIP5Kalpha）及其脂质产物磷脂酰肌醇4,5-双磷酸（PI [4,5] P（2））调节重要的细胞表面功能。在这里，我们报告脂多糖（LPS）以时间和浓度依赖性的方式在小胶质细胞中显着增强PIP5Kalpha mRNA和蛋白质表达水平。此外，LPS刺激导致质膜中PI（4,5）P（2）的强劲增加，通过PI（4,5）P（2）免疫染色或PI（4,5）P（2）成像证明使用PI（4,5）P（2）特异性探针tubby（R332H），与黄色荧光蛋白融合。磷脂酰肌醇3-激酶，p38丝裂原活化蛋白激酶（MAPK），p42 / 44 MAPK和c-Jun N端激酶信号通路抑制剂明显降低了PIP5Kalpha的表达，表明这些通路对于LPS诱导的PIP5Kalpha表达是必需的。此外，抑制核因子-κB和Sp1转录因子会干扰LPS诱导的PIP5Kalpha上调。 PI（4,5）P（2）传递到小胶质细胞增加了白介素1beta和肿瘤坏死因子α的表达。这些发现表明，在LPS刺激的小胶质细胞中，PIP5Kalpha上调和PI（4,5）P（2）的升高可能会积极调节小胶质细胞的炎症反应。

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