Brca1 Is Upregulated by 5-Aza-CdR and Promotes DNA Repair and Cell Survival, and Inhibits Neurite Outgrowth in Rat Retinal Neurons.

Brca1 Is Upregulated by 5-Aza-CdR and Promotes DNA Repair and Cell Survival, and Inhibits Neurite Outgrowth in Rat Retinal Neurons.
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Brca1 受 5-Aza-CdR 上调,促进 DNA 修复和细胞存活,并抑制大鼠视网膜神经元中的神经突生长

DOI:
10.3390/ijms19041214
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发表时间:
2018-04-17
影响因子:
5.6
通讯作者:
Zhuang J
Zhuang J
中科院分区:
生物学2区
文献类型:
--
作者:
Wang Q;Xu L;Chen P;Xu Z;Qiu J;Ge J;Yu K;Zhuang J

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先前的研究报道,Brca1在中枢神经系统(CNS)的发育中起着“铰链”的作用。然而,Brca1在大鼠视网膜神经元中的确切作用尚不清楚。在这里,我们发现Brca1在成人视网膜中发育下调和沉默。5-Aza-2 ' -脱氧胞苷(5-Aza-CdR)处理后,Brca1在大鼠原代视网膜神经元中表达上调。此外,5-Aza-CdR和转基因Brca1对Brca1的上调促进了电离辐射(IR)暴露后基因组的稳定性和细胞活力的提高。此外,转基因Brca1显著抑制视网膜神经元的神经突生长,这表明Brca1沉默促进细胞分化并决定神经元形态。综上所述,我们的结果揭示了Brca1在视网膜发育中的生物学功能。
Previous studies have reported that Brca1 acts as a “hinge” in the development of the central nervous system (CNS). However, the precise role of Brca1 in rat retinal neurons remains unclear. Here, we found that Brca1 is developmentally downregulated and silenced in adult retina. Brca1 was upregulated in rat primary retinal neurons by 5-Aza-2′-deoxycytidine (5-Aza-CdR) treatment. Moreover, the upregulation of Brca1 by both 5-Aza-CdR and transgenic Brca1 promoted genomic stability and improved cell viability following exposure to ionizing radiation (IR). Furthermore, transgenic Brca1 significantly inhibited neurite outgrowth of retinal neurons, which implicates that Brca1 silencing promotes cell differentiation and determines neuronal morphology. Taken together, our results reveal a biological function of Brca1 in retinal development.
在发育,重编程和肿瘤发生过程中,视网膜的动态表观遗传景观。
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