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人软骨细胞暴露于 T-2 毒素和脱氧雪腐镰刀菌烯醇后与硒相关基因的表达谱。

Expression Profiles of Selenium-Related Genes in Human Chondrocytes Exposed to T-2 Toxin and Deoxynivalenol.

机构信息

School of Nursing, Health Science Center, Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, People's Republic of China.

School of Public Health, Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, People's Republic of China.

出版信息

Biol Trace Elem Res. 2019 Aug;190(2):295-302. doi: 10.1007/s12011-018-1560-2. Epub 2018 Nov 7.

DOI:10.1007/s12011-018-1560-2
PMID:30406490
Abstract

The combination of excess mycotoxin exposure and selenium deficiency has been widely considered as a cause of Kashin-Beck disease (KBD). The present study aimed to investigate the expression profiles of selenium-related genes in human chondrocytes after exposure to T-2 toxin and deoxynivalenol (DON) and to preliminarily identify the potential biological functions of the identified genes. Gene expression profiling was performed on human chondrocytes treated with 0.01 μg/ml T-2 toxin and 1.0 μg/ml DON by using Affymetrix Human Gene Arrays. The 1660 selenium-related genes were derived from the Comparative Toxicogenomics Database. Gene-term enrichment analysis was conducted by the DAVID gene annotation tool. Our results showed that 69 and 191 selenium-related genes were differentially expressed after T-2 toxin and DON treatment, respectively. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that these identified genes were involved in various biological functions, such as the GO terms in response to oxidative stress, cell cycle arrest, and apoptotic process and the KEGG metabolic, FoxO signaling, and p53 signaling pathways. Our results may help explain the mechanisms of interaction between mycotoxins and selenium following human chondrocyte damage and reveal the potential roles of environmental risk factors in cartilage lesions during KBD development.

摘要

黄曲霉毒素暴露过量与硒缺乏的联合作用被广泛认为是大骨节病(KBD)的病因之一。本研究旨在探讨 T-2 毒素和脱氧雪腐镰刀菌烯醇(DON)暴露后人软骨细胞中与硒相关基因的表达谱,并初步鉴定鉴定基因的潜在生物学功能。采用 Affymetrix Human Gene Arrays 对 0.01μg/ml T-2 毒素和 1.0μg/ml DON 处理的人软骨细胞进行基因表达谱分析。从比较毒理学基因组数据库中获得了 1660 个与硒相关的基因。通过 DAVID 基因注释工具进行基因-术语富集分析。结果显示,T-2 毒素和 DON 处理后分别有 69 个和 191 个与硒相关的基因表达差异。GO 和 KEGG 通路分析显示,这些鉴定的基因参与了各种生物学功能,如GO 术语中的氧化应激反应、细胞周期停滞和凋亡过程,以及 KEGG 代谢、FoxO 信号和 p53 信号通路。我们的研究结果可能有助于解释人类软骨细胞损伤后真菌毒素与硒相互作用的机制,并揭示环境危险因素在 KBD 发病过程中对软骨损伤的潜在作用。

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