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大鼠视神经损伤后视网膜 Müller 胶质细胞的激活:与转录起始因子 IIb 的时空相关性。

Müller glia cells activation in rat retina after optic nerve injury: spatiotemporal correlation with transcription initiation factor IIb.

机构信息

Department of Ophthalmology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, 226001, People's Republic of China.

出版信息

J Mol Neurosci. 2013 Sep;51(1):37-46. doi: 10.1007/s12031-012-9941-z. Epub 2013 Jan 9.

DOI:10.1007/s12031-012-9941-z
PMID:23297010
Abstract

Transcription initiation factor IIB (TFIIB) is an ideal factor to localize core promoters and plays a central role in the assembly of the pre-initiation complex. Previous studies showed that the assembly of TFIIB played an important role in rat ischemic brain injury. To elucidate the expression and possible functions of TFIIB in retina lesion and repair, we performed an optic nerve crush (ONC) model in adult rats. Western blot analysis and immunohistochemistry showed a significant upregulation of TFIIB in retina after ONC. Immunofluorescent labeling indicated that TFIIB was localized mainly in the Müller glia cells (MGCs); colocalization of TFIIB and proliferating cell nuclear antigen (PCNA) in the injured retina suggested that TFIIB might participate in MGCs proliferation. In addition, we also examined the expression of the retinal progenitor markers (Nestin and Pax6) whose changes were correlated with the expression of TFIIB. In vitro, we induced MGCs differentiation with brain nerve growth factor (BNGF) and found that TFIIB expression was increased in the differentiated process, which was collected with the expression of PCNA, Nestin, and Pax6. Additionally, knocking TFIIB down with siRNA inhibited the expression of PCNA, Nestin, and Pax6. Collectively, we hypothesized ONC-induced upregulation of TFIIB in the retina was associated with MGCs activation and differentiation.

摘要

转录起始因子 IIB(TFIIB)是一种理想的定位核心启动子的因子,在起始前复合物的组装中发挥核心作用。先前的研究表明,TFIIB 的组装在大鼠缺血性脑损伤中发挥了重要作用。为了阐明 TFIIB 在视网膜病变和修复中的表达和可能的功能,我们在成年大鼠中建立了视神经挤压(ONC)模型。Western blot 分析和免疫组织化学显示,ONC 后视网膜中 TFIIB 的表达显著上调。免疫荧光标记表明,TFIIB 主要定位于 Muller 胶质细胞(MGCs)中;在受损的视网膜中 TFIIB 与增殖细胞核抗原(PCNA)的共定位表明,TFIIB 可能参与 MGCs 的增殖。此外,我们还检测了视网膜祖细胞标志物(Nestin 和 Pax6)的表达,其变化与 TFIIB 的表达相关。在体外,我们用脑源性神经生长因子(BNGF)诱导 MGCs 分化,发现 TFIIB 的表达在分化过程中增加,与 PCNA、Nestin 和 Pax6 的表达相关。此外,用 siRNA 敲低 TFIIB 抑制了 PCNA、Nestin 和 Pax6 的表达。综上所述,我们假设 ONC 诱导的视网膜中 TFIIB 的上调与 MGCs 的激活和分化有关。

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本文引用的文献

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J Mol Neurosci. 2013 Mar;49(3):491-8. doi: 10.1007/s12031-012-9865-7. Epub 2012 Aug 7.
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Small RNAs targeting transcription start site induce heparanase silencing through interference with transcription initiation in human cancer cells.靶向转录起始位点的小 RNA 通过干扰人癌细胞中的转录起始诱导乙酰肝素酶沉默。
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Molecular basis of Rrn3-regulated RNA polymerase I initiation and cell growth.
载脂蛋白B mRNA编辑酶催化多肽样蛋白1促进神经毒性诱导的米勒胶质细胞去分化。
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Upregulation of SYF2 Relates to Retinal Ganglion Cell Apoptosis and Retinal Glia Cell Proliferation After Light-Induced Retinal Damage.SYF2的上调与光诱导视网膜损伤后视网膜神经节细胞凋亡及视网膜胶质细胞增殖有关。
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The expression changes of myelin and lymphocyte protein (MAL) following optic nerve crush in adult rats retinal ganglion cells.成年大鼠视网膜神经节细胞视神经挤压伤后髓鞘和淋巴细胞蛋白(MAL)的表达变化
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A new paradigm for transcription factor TFIIB functionality.转录因子TFIIB功能的一种新范式。
Sci Rep. 2014 Jan 20;4:3664. doi: 10.1038/srep03664.
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Increased expression of transcription initiation factor IIB after rat traumatic brain injury.大鼠创伤性脑损伤后转录起始因子 IIB 的表达增加。
J Mol Histol. 2011 Jun;42(3):265-71. doi: 10.1007/s10735-011-9330-x. Epub 2011 May 5.
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