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紫外线B照射后人晶状体上皮细胞系中蛋白质组和泛素化组变化的综合分析

Comprehensive Profiling of Proteome and Ubiquitome Changes in Human Lens Epithelial Cell Line after Ultraviolet-B Irradiation.

作者信息

Chen Xiaojuan, Li Pengfei, Zhang Guowei, Kang Lihua, Qin Bai, Mao Xinmu, Qin Miaomiao, Cao Yu, Wang Ying, Guan Huaijin

机构信息

Eye Institute, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226000, China.

出版信息

ACS Omega. 2020 Dec 7;5(50):32171-32182. doi: 10.1021/acsomega.0c03088. eCollection 2020 Dec 22.

DOI:10.1021/acsomega.0c03088
PMID:33376855
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7758888/
Abstract

Ultraviolet-B (UVB) is a recognized risk factor for age-related cataract (ARC) and can cause various changes, including ubiquitination, in lens epithelial cells (LECs). However, the relationship between ubiquitination and ARC is unclear. Herein, we used UVB-irradiated human lens epithelial cell line (SRA01/04) representing the cell model of ARC to investigate the profile changes in the proteome and ubiquitome. A total of 552 differentially expressed proteins (DEPs) and 871 differentially ubiquitinated proteins (DUPs) were identified, and 9 ubiquitination motifs were found. Bioinformatics analysis revealed diverse pathways and biological processes of differential proteins and several DNA damage repair proteins that were potentially mediated via ubiquitin-proteasome pathway. We validated the decreased protein expression of DNA-directed RNA polymerase II subunit RPB2 (POLR2B) in both human cataract capsule tissues and UVB-treated SRA01/04 cells and found that treatment with proteasome inhibitor (MG-132) could reverse the protein level of POLR2B in UVB-irradiated SRA01/04 cells. Our data provide novel information regarding protein expressions and ubiquitination modifications in UVB-induced oxidative damage model. This study might offer a cell-level reference to further investigate the pathogenesis of ARC.

摘要

紫外线B（UVB）是年龄相关性白内障（ARC）的一个公认风险因素，可在晶状体上皮细胞（LEC）中引起包括泛素化在内的各种变化。然而，泛素化与ARC之间的关系尚不清楚。在此，我们使用代表ARC细胞模型的UVB照射人晶状体上皮细胞系（SRA01/04）来研究蛋白质组和泛素组的谱变化。共鉴定出552种差异表达蛋白（DEP）和871种差异泛素化蛋白（DUP），并发现了9种泛素化基序。生物信息学分析揭示了差异蛋白的多种途径和生物学过程，以及几种可能通过泛素-蛋白酶体途径介导的DNA损伤修复蛋白。我们验证了DNA指导的RNA聚合酶II亚基RPB2（POLR2B）在人白内障囊膜组织和UVB处理的SRA01/04细胞中的蛋白表达均降低，并发现用蛋白酶体抑制剂（MG-132）处理可逆转UVB照射的SRA01/04细胞中POLR2B的蛋白水平。我们的数据提供了关于UVB诱导的氧化损伤模型中蛋白质表达和泛素化修饰的新信息。本研究可能为进一步研究ARC的发病机制提供细胞水平的参考。

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