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首页> 外文期刊>The European Journal of Neuroscience >Glial fibrillary acidic protein gene promoter is differently modulated by transforming growth factor-beta 1 in astrocytes from distinct brain regions.
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Glial fibrillary acidic protein gene promoter is differently modulated by transforming growth factor-beta 1 in astrocytes from distinct brain regions.

机译：胶质纤维酸性蛋白基因启动子通过转化来自不同大脑区域的星形胶质细胞中的生长因子-β1来不同地调节。

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Abstract The expression of glial fibrillary acidic protein (GFAP), the major intermediate filament protein of mature astrocytes, is regulated under developmental and pathological conditions. Recently, we have investigated GFAP gene modulation by using a transgenic mouse bearing part of the GFAP gene promoter linked to the beta-galactosidase reporter gene. We demonstrated that cerebral cortex neurons activate the GFAP gene promoter, inducing transforming growth factor-beta 1 (TGF-beta1) secretion by astrocytes. Here, we report that cortical neurons or conditioned medium derived from them do not activate the GFAP gene promoter of transgenic astrocytes derived from midbrain and cerebellum suggesting a neuroanatomical regional specificity of this phenomenon. Surprisingly, they do induce synthesis of TGF-beta1 by these cells. Western blot and immunocytochemistry assays revealed wild distribution of TGF receptor in all subpopulations of astrocytes and expression of TGF-beta1 in neurons derived from all regions, thus indicating that the unresponsiveness of the cerebellar and midbrain GFAP gene to TGF-beta1 is not due to a defect in TGF-beta1 signalling. Together, our data highlight the great complexity of neuron-glia interactions and might suggest a distinct mechanism underlying modulation of the GFAP gene in the heterogeneous population of astrocytes throughout the central nervous system.
机译：摘要成熟的星形胶质细胞主要的中间丝蛋白胶质原纤维酸性蛋白（GFAP）的表达受发育和病理条件的调节。最近，我们已经研究了通过使用带有一部分与β-半乳糖苷酶报道基因连接的GFAP基因启动子的转基因小鼠来调节GFAP基因。我们证明了大脑皮层神经元激活GFAP基因启动子，诱导星形胶质细胞分泌转化生长因子-β1（TGF-β1）分泌。在这里，我们报告皮质神经元或从它们衍生的条件培养基不能激活源自中脑和小脑的转基因星形胶质细胞的GFAP基因启动子，提示此现象的神经解剖学区域特异性。令人惊讶的是，它们确实诱导了这些细胞合成TGF-β1。 Western印迹和免疫细胞化学分析显示，星形胶质细胞所有亚群中TGF受体均呈野生型分布，所有区域的神经元中TGF-β1均表达，因此表明小脑和中脑GFAP基因对TGF-β1的无反应性不是由于TGF-beta1信号传导缺陷。总之，我们的数据突出了神经元-神经胶质细胞相互作用的巨大复杂性，并可能暗示了在整个中枢神经系统异质星形胶质细胞群体中GFAP基因调控的独特机制。

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