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首页> 外文期刊>The European Journal of Neuroscience >Neuro-glia interaction effects on GFAP gene: a novel role for transforming growth factor-beta1.
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Neuro-glia interaction effects on GFAP gene: a novel role for transforming growth factor-beta1.

机译：神经胶质细胞相互作用对GFAP基因的影响：转化生长因子-beta1的新作用。

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摘要

Central nervous system (CNS) development is highly guided by microenvironment cues specially provided by neuron-glia interactions. By using a transgenic mouse bearing part of the gene promoter of the astrocytic maturation marker GFAP (glial fibrillary acidic protein) linked to the beta-galactosidase (beta-Gal) reporter gene, we previously demonstrated that cerebral cortical neurons increase transgenic beta-Gal astrocyte number and activate GFAP gene promoter by secretion of soluble factors in vitro. Here, we identified TGF-beta1 as the major mediator of this event. Identification of TGF-beta1 in neuronal and astrocyte extracts revealed that both cell types might synthesize this factor, however, addition of neurons to astrocyte monolayers greatly increased TGF-beta1 synthesis and secretion by astrocytes. Further, by exploiting the advantages of cell culture system we investigated the influence of neuron and astrocyte developmental stage on such interaction. We demonstrated that younger neurons derived from 14 embryonic days wild-type mice were more efficient in promoting astrocyte differentiation than those derived from 18 embryonic days mice. Similarly, astrocytes also exhibited timed-schedule developed responsiveness to neuronal influence with embryonic astrocytes being more responsive to neurons than newborn and late postnatal astrocytes. RT-PCR assays identified TGF-beta1 transcripts in young but not in old neurons, suggesting that inability to induce astrocyte differentiation is related to TGF-beta1 synthesis and secretion. Our work reveals an important role for neuron-glia interactions in astrocyte development and strongly implicates the involvement of TGF-beta1 in this event.
机译：中枢神经系统（CNS）的发展在很大程度上由神经元-胶质细胞相互作用提供的微环境线索指导。通过使用带有星形胶质细胞成熟标记GFAP（神经胶质纤维酸性蛋白）的基因启动子的转基因小鼠，该基因启动子与β-半乳糖苷酶（β-Gal）报道基因相连，我们以前证明了大脑皮层神经元会增加转基因β-Gal星形胶质细胞通过体外分泌可溶性因子激活GFAP基因启动子。在这里，我们确定TGF-beta1是此事件的主要介体。神经元和星形胶质细胞提取物中TGF-β1的鉴定表明，两种细胞都可能合成该因子，但是，向星形胶质细胞单层添加神经元极大地增加了星形胶质细胞的TGF-β1合成和分泌。此外，通过利用细胞培养系统的优势，我们研究了神经元和星形胶质细胞发育阶段对这种相互作用的影响。我们证明，来自14个胚胎天野生型小鼠的年轻神经元比来自18个胚胎天小鼠的神经元在促进星形胶质细胞分化方面更有效。同样，星形胶质细胞还表现出对神经元影响的定时发展，与新生和出生后的星形胶质细胞相比，胚胎星形胶质细胞对神经元的响应性更高。逆转录-聚合酶链反应（RT-PCR）分析鉴定出年轻的神经元中的TGF-beta1转录本，而老年神经元中没有，这表明无法诱导星形胶质细胞分化与TGF-beta1的合成和分泌有关。我们的工作揭示了神经元-胶质细胞相互作用在星形胶质细胞发育中的重要作用，并强烈暗示TGF-beta1参与此事件。

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