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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。

Upregulation of SYF2 Relates to Retinal Ganglion Cell Apoptosis and Retinal Glia Cell Proliferation After Light-Induced Retinal Damage.

作者信息

Sang Aimin, Yang Xiaowei, Chen Hui, Qin Bai, Zhu Manhui, Dai Ming, Zhu Rongrong, Liu Xiaojuan

机构信息

Department of Ophthalmology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.

出版信息

J Mol Neurosci. 2015 Jun;56(2):480-90. doi: 10.1007/s12031-015-0534-5. Epub 2015 May 6.

Abstract

SYF2 (SYF2 homologue, RNA splicing factor), also known as CCNDBP1-interactor or p29, belongs to the SYF2 family, which are involved in pre-mRNA splicing and cell cycle progression. Accumulating evidences demonstrate that SYF2 exerted multiple effects including pro-apoptosis, cell differentiation, and glial activation in the pathogenesis of various experimental central nervous system (CNS) diseases. However, SYF2 expression and functions in the retina are still with limited acquaintance. To investigate whether SYF2 was involved in retinal degeneration, we performed a light-induced retinal damage model in adult rats. The SYF2 protein expression was dramatically upregulated after retinal damage. Besides that, SYF2 localized in the retinal ganglion cell (RGC) layer (GCL), inner unclear layer (INL), and outer nuclear layer (ONL) after light exposure. In addition, the expression of cyclin D1, CDK4, and active caspase-3 was parallel with SYF2. We also found the co-localization of SYF2 with active caspase-3, PCNA, and CD11b. Collectively, SYF2 might participate in RGC apoptosis and retinal glia cell proliferation after light-induced retinal damage.

摘要

SYF2(SYF2同源物,RNA剪接因子),也被称为CCNDBP1相互作用蛋白或p29,属于SYF2家族,该家族参与前体mRNA剪接和细胞周期进程。越来越多的证据表明,SYF2在各种实验性中枢神经系统(CNS)疾病的发病机制中发挥多种作用,包括促凋亡、细胞分化和神经胶质细胞激活。然而,人们对SYF2在视网膜中的表达和功能仍知之甚少。为了研究SYF2是否参与视网膜变性,我们在成年大鼠中建立了光诱导视网膜损伤模型。视网膜损伤后,SYF2蛋白表达显著上调。除此之外,光照后SYF2定位于视网膜神经节细胞(RGC)层(GCL)、内核层(INL)和外核层(ONL)。此外,细胞周期蛋白D1、细胞周期蛋白依赖性激酶4(CDK4)和活化的半胱天冬酶-3的表达与SYF2平行。我们还发现SYF2与活化的半胱天冬酶-3、增殖细胞核抗原(PCNA)和CD11b共定位。总体而言,SYF2可能参与光诱导视网膜损伤后的RGC凋亡和视网膜神经胶质细胞增殖。

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