PLoS Genet:需要Müller神经胶质的PRSS56分子可以维持眼睛轴向生长并防止屈光不正

2018-03-14 cuiguizhong MedSci原创

美国加州大学旧金山分校眼科学系的Paylakhi S近日在PLoS Genet发表了一项工作,他们使用不同基因型小鼠模型来证明Prss56突变导致眼尺寸减小和远视。

美国加州大学旧金山分校眼科学系的Paylakhi S近日在PLoS Genet发表了一项工作,他们使用不同基因型小鼠模型来证明Prss56突变导致眼尺寸减小和远视。

光焦度与眼轴长度之间的不匹配可以引起屈光不正。未矫正的屈光不正是造成全球视力丧失的最常见原因,也是导致失明的第二大原因。虽然已知视网膜在调节眼部生长和屈光发育方面起着关键作用,但所涉及的确切因素和机制尚不清楚。作者之前的研究已经确定了分泌型丝氨酸蛋白酶PRSS56在眼部大小测定中的作用,并且PRSS56突变体与远视和近视的病因有关,这突出了它在屈光不正发育中的重要性。在这里,他们使用不同基因型小鼠模型来证明Prss56突变导致眼尺寸减小和远视。

使用条件基因靶向策略,他们显示来自Müller神经胶质细胞的PRSS56有助于眼生长,暗示在眼尺寸测定中新的视网膜细胞类型具有重要作用。同时,他们证明PRSS56的持续活动需要跨越眼睛睁开前和眼睛睁开后不同发育阶段期间以确保最佳的眼部生长。因此,他们的小鼠数据提供了在产前和产后阶段促进人眼生长的分子机制。最后,他们证明Prss56的遗传失活可以拯救由Egr1中的无效突变引起的小鼠近视模型中的眼轴伸长。

总体而言,他们的研究结果将PRSS56确定为调节眼球生长的潜在治疗靶点,希望能够预防或减缓近视的发生。

原文出处:

Paylakhi, S., et al., Muller glia-derived PRSS56 is required to sustain ocular axial growth and prevent refractive error. PLoS Genet, 2018. 14(3): p. e1007244.

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    2018-07-27 canlab
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    2018-09-06 cy0324
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    2018-10-19 kzlchina
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