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在N-甲基-D-天冬氨酸诱导的视神经挤压损伤过程中，靶向Nogo受体的RNA干扰增强了小鼠视网膜神经节细胞的存活和增殖。

RNAi targeting Nogo Receptor enhanced survival and proliferation of murine retinal ganglion cells during N-methyl-D-aspartate-induced optic nerve crush.

作者信息

Zeng Kun, Zhong Bo, Shen Xiao-Li, Fang Min, Lin Bao-Tao, Ma Da-Hui

机构信息

Key Laboratory of Ophthalmology, Shenzhen Eye Hospital, Ophthalmology College of Shenzhen University, Shenzhen 518000, P.R. China.

Department of Stomatology, Shenzhen Second People's Hospital, Shenzhen 518000, P.R. China.

出版信息

Oncotarget. 2017 Apr 21;8(39):65009-65021. doi: 10.18632/oncotarget.17351. eCollection 2017 Sep 12.

DOI:10.18632/oncotarget.17351
PMID:29029408
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5630308/
Abstract

We investigated the effects of lentivirus-mediated RNAi targeting of Nogo Receptor () on the proliferation and survival of murine retinal ganglion cells (mRGCs) and . Cultured mRGCs and C57BL/6 male mice were divided into 4 experimental groups: blank, model [100 μM N-methyl-D-aspartate (NMDA)], nscRNA (100 μM NMDA+ nscRNA vectors) and siNgR (100 μM NMDA+ siNgR vectors). CCK-8 and flow cytometry analyses revealed that silencing enhanced proliferation, cell cycling and survival of NMDA-treated mRGCs. H&E staining showed that silencing enhanced mRGC cell density and reduced angiogenesis in NMDA-treated retinal tissues. TUNEL assays showed that mRGC apoptosis was significantly diminished by silencing in NMDA-treated retinal tissues. Western blotting and qRT-PCR analysis in NMDA-treated mRGCs and murine retinal tissues revealed that silencing resulted in downregulation of RhoA signaling (RhoA and ROCK2). Western blotting showed that levels of activated Bax and cleaved caspase 3 were decreased, while Bcl-2 and pro-caspase 3 were increased in NMDA-treated mRGCs and murine retinal tissues, which corroborated the decreased apoptosis. These findings indicate that gene silencing increases proliferation and survival of mRGCs in NMDA-treated murine retinas, which suggests a potential for therapeutic application to preventing optic nerve damage.

摘要

我们研究了慢病毒介导的针对Nogo受体（）的RNA干扰对小鼠视网膜神经节细胞（mRGCs）增殖和存活的影响。将培养的mRGCs和C57BL/6雄性小鼠分为4个实验组：空白组、模型组[100μM N-甲基-D-天冬氨酸（NMDA）]、非特异性RNA组（100μM NMDA +非特异性RNA载体）和siNgR组（100μM NMDA + siNgR载体）。CCK-8和流式细胞术分析显示，沉默可增强NMDA处理的mRGCs的增殖、细胞周期进程和存活能力。苏木精-伊红染色显示，沉默可提高NMDA处理的视网膜组织中的mRGC细胞密度并减少血管生成。TUNEL检测显示，在NMDA处理的视网膜组织中，沉默可显著减少mRGC凋亡。对NMDA处理的mRGCs和小鼠视网膜组织进行的蛋白质免疫印迹和qRT-PCR分析显示，沉默导致RhoA信号通路（RhoA和ROCK2）下调。蛋白质免疫印迹显示，在NMDA处理的mRGCs和小鼠视网膜组织中，活化的Bax和裂解的caspase 3水平降低，而Bcl-2和前体caspase 3水平升高，这证实了凋亡减少。这些发现表明，沉默基因可增加NMDA处理的小鼠视网膜中mRGCs的增殖和存活，这提示其在预防视神经损伤的治疗应用中具有潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ec2/5630308/46914b18c4a0/oncotarget-08-65009-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ec2/5630308/2819519b5cf3/oncotarget-08-65009-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ec2/5630308/4a5e51654beb/oncotarget-08-65009-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ec2/5630308/11e2645e6a16/oncotarget-08-65009-g007.jpg
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J Ethnopharmacol. 2016 Dec 24;194:1032-1042. doi: 10.1016/j.jep.2016.11.005. Epub 2016 Nov 8.
2
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J Ethnopharmacol. 2016 Aug 22;190:301-12. doi: 10.1016/j.jep.2016.06.017. Epub 2016 Jun 8.
3
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