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首页> 外文期刊>Cytotechnology >Atoh7 promotes retinal Müller cell differentiation into retinal ganglion cells
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Atoh7 promotes retinal Müller cell differentiation into retinal ganglion cells

机译:Atoh7促进视网膜Müller细胞分化为视网膜神经节细胞

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Glaucoma is one of the leading eye diseases due to the death of retinal ganglion cells. Increasing evidence suggests that retinal Müller cells exhibit the characteristics of retinal progenitor cells and can differentiate to neurons in injured retinas under certain conditions. However, the number of ganglion cells differentiated from retinal Müller cells falls far short of therapeutic needs. This study aimed to promote the differentiation of retinal Müller cells into ganglion cells by introducing Atoh7 into the stem cells dedifferentiated from retinal Müller cells. Rat retinal Müller cells were isolated and dedifferentiated into stem cells, which were transfected with PEGFP-N1 or PEGFP-N1-Atoh7 vector, and then further induced to differentiate into ganglion cells. The proportion of ganglion cells differentiated from Atoh7-tranfected stem cells was significantly higher than that of control transfected or untransfected cells. In summary, Atoh7 promotes the differentiation of retinal Müller cells into retinal ganglion cells. This may open a new avenue for gene therapy of glaucoma by promoting optic nerve regeneration.
机译:由于视网膜神经节细胞死亡,青光眼是主要的眼部疾病之一。越来越多的证据表明,视网膜Müller细胞具有视网膜祖细胞的特征,并且在某些情况下可以分化为受损视网膜中的神经元。但是,从视网膜Müller细胞分化出的神经节细胞数量远远不能满足治疗需求。这项研究旨在通过将Atoh7引入从视网膜Müller细胞去分化的干细胞中来促进视网膜Müller细胞向神经节细胞的分化。分离大鼠视网膜Müller细胞并将其去分化为干细胞,将其用PEGFP-N1或PEGFP-N1-Atoh7载体转染,然后进一步诱导分化为神经节细胞。从Atoh7转染的干细胞分化出的神经节细胞的比例显着高于对照转染或未转染的细胞。总之,Atoh7促进视网膜Müller细胞分化为视网膜神经节细胞。通过促进视神经再生,这可能为青光眼的基因治疗开辟新途径。

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