TGF-β1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia
TGF-β1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia
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DOI：
10.1016/s0165-5728(02)00354-5
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发表时间：
2002-12-01
影响因子：
3.3
通讯作者：
Harrison, JK
中科院分区：
文献类型：
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作者：
Chen, SZ;Luo, DF;Harrison, JK
周围神经横断后，损伤的颜面运动核内CX3CR1和tgf - β 1呈时间依赖性增加。为了探讨tgf - β 1与CX3CR1在中枢神经系统中的关系，我们检测了tgf - β 1对大鼠小胶质细胞原代培养中CX3CR1 mRNA、蛋白和分形因子依赖性信号转导级联的影响。tgf - β 1增加了CX3CR1 mRNA、i -125 fractalkine结合位点的稳态水平，减弱了fractalkine刺激的ERK 1/2磷酸化。tgf - β 1未改变CX3CR1 mRNA的半衰期，并且在大鼠CX3CR1启动子中鉴定了两个潜在的Smad结合元件（SBEs）。tgf - β 1可能将分形因子依赖的信号从ERK1/2的激活转移到其他途径和/或可能为小胶质细胞更强烈地粘附神经元提供机制。(C) 2002 Elsevier Science B.V.版权所有
Following peripheral nerve transection, CX3CR1 and TGF-beta1 are increased in a time-dependent manner within the injured facial motor nucleus. To explore the relationship between TGF-beta1 and CX3CR1 in the CNS, the effects of TGF-beta1 on CX3CR1 mRNA, protein and fractalkine-dependent stimulation of signal transduction cascades in primary cultures of rat microglia were examined. TGF-beta1 increased steady state levels of CX3CR1 mRNA, I-125-fractalkine binding sites and blunted fractalkine-stimulated ERK 1/2 phosphorylation. The half-life of CX3CR1 mRNA was unaltered by TGF-beta1 and two potential Smad binding elements (SBEs) were identified in the rat CX3CR1 promoter. TGF-beta1 may shift fractalkine-dependent signaling away from activation of ERK1/2 towards other pathways and/or may provide a mechanism for microglia to more strongly adhere to neurons. (C) 2002 Elsevier Science B.V. All rights reserved.