视网膜外植体培养中突触神经胶质细胞发育过程中的MAPK信号传导。

Samuel Shao-Min Zhang, Hong Li, Ping Huang, Lucy Xi Lou, Xin-Yuan Fu, Colin J Barnstable
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引用次数: 6

摘要

勒细胞是唯一一种从视网膜神经上皮生成的胶质细胞类型。这种细胞类型控制正常的视网膜稳态,并被认为发挥神经保护作用。最近的证据表明,哺乳动物的 ller细胞可以在损伤或疾病后去分化并返回到祖细胞或干细胞阶段。在体内探索m ller细胞分化和增殖的分子机制将为操纵m ller细胞功能提供必要的信息。信号转导通路调节 ller细胞的反应和活动是其细胞机制的重要组成部分。在这项研究中,我们重点研究了丝裂原活化蛋白激酶(MAPK)信号通路在突触神经胶质细胞分化和增殖中的作用。我们发现MAPK和STAT3信号通路都存在于突触神经胶质细胞发育过程中。睫状体神经营养因子(CNTF)刺激的神经胶质细胞增殖与早期发育阶段有关。特异性抑制MAPK磷酸化在CNTF刺激或不刺激的情况下显著减少了突触神经胶质细胞的数量。这些结果表明,MAPK信号转导通路在视网膜发育过程中突触神经胶质细胞的形成中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MAPK signaling during Müller glial cell development in retina explant cultures.

The Müller cell is the only glial cell type generated from the retinal neuroepithelium. This cell type controls normal retina homeostasis and has been suggested to play a neuroprotective role. Recent evidence suggests that mammalian Müller cells can de-differentiate and return to a progenitor or stem cell stage following injury or disease. In vivo exploration of the molecular mechanisms of Müller cell differentiation and proliferation will add essential information to manipulate Müller cell functions. Signal transduction pathways that regulate Müller cell responses and activity are a critical part of their cellular machinery. In this study, we focus on mitogen-activated protein kinase (MAPK) signaling pathway during Müller glial cell differentiation and proliferation. We found that both MAPK and STAT3 signaling pathways are present during Müller glial cell development. Ciliary neurotrophic factor (CNTF)-stimulated Müller glial cell proliferation is associated with early developmental stages. Specific inhibition of MAPK phosphorylation significantly reduced the number of Müller glial cells with or without CNTF stimulation. These results suggested that the MAPK signal transduction pathway is important in the formation of Müller glial cells during retina development.

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