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Sox2 Knockdown in the Neonatal Retina Causes Cell Fate to Switch from Amacrine to Bipolar
Brain Research ( IF 2.9 ) Pub Date : 2021-01-07 , DOI: 10.1016/j.brainres.2020.147265
Yunzepeng Li 1 , Yumeng Shen 2 , Danrui Cai 1 , Yin Shen 3
Affiliation  

Transcription factor Sox2 is widely recognized for its critical roles in the nervous system, including the neural retina. Here, we aimed to reveal the function of Sox2 in the process of mouse postnatal development. After the suppression of Sox2 at P0, there was an increase number in bipolar cells but a decrease in amacrine cells. Inhibited Sox2 expression also led to decreased visual function. Furthermore, we found a distinctive type of retinal cells expressing the characteristic proteins of both bipolar cells and amacrine cells at P6, which may be an intermediate state in which amacrine cells were transforming into bipolar cells. Transcription factors associated with the development of bipolar cells and amacrine cells also support those changes. Our work indicated that inhibition of Sox2 could change cell fate by affecting transcription factors in the development of bipolar cells and amacrine cells, may provide new directions for the study and treatment of retinal genetic diseases and retinal dysplasia.



中文翻译:

新生儿视网膜中的 Sox2 敲低导致细胞命运从无长突转变为双极

转录因子 Sox2 因其在神经系统(包括神经视网膜)中的关键作用而被广泛认可。在这里,我们旨在揭示 Sox2 在小鼠出生后发育过程中的功能。在 P0 抑制 Sox2 后,双极细胞数量增加,但无长突细胞数量减少。抑制的 Sox2 表达也导致视觉功能下降。此外,我们发现一种独特类型的视网膜细胞在 P6 表达双极细胞和无长突细胞的特征蛋白,这可能是无长突细胞转化为双极细胞的中间状态。与双极细胞和无长突细胞发育相关的转录因子也支持这些变化。

更新日期:2021-01-07
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