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支气管上皮细胞对钒暴露反应的基因表达。

Gene Expression in Bronchial Epithelial Cell Responses to Vanadium Exposure.

机构信息

College of Animal Science, Anhui Science and Technology University, Fengyang, 233100, China.

Biological Applications Department, Nuclear Research Center, Egyptian Atomic Energy Authority, Abu-Zaabal, 13759, Egypt.

出版信息

Biol Trace Elem Res. 2023 Aug;201(8):3774-3790. doi: 10.1007/s12011-022-03461-7. Epub 2022 Nov 5.

Abstract

Vanadium exposure has the adverse effect on lung function in human, whereas the detailed mechanisms of vanadium exposure-induced pulmonary toxicity are limited. Hence, the present study aimed to investigate the hub genes and signaling pathways related to sodium metavanadate (SMV)-induced pulmonary toxicity. The transcript expression profile GSE36684 downloaded from Gene Expression Omnibus contained eight human bronchial epithelial cell (HBEC) samples including five SMV-treated and three control HBEC samples. Totally 455 differentially expressed genes (DEGs) were screened, especially 201 and 254 genes were up- and down-regulated in the HBECs treated with SMV. Gene ontology analysis suggested that the DEGs were mainly involved in signal transduction, the response to drug, cell proliferation, adhesion, and migration. Pathway analysis demonstrated that the DEGs were primarily participated in NF-κB, Wnt, MAPK, and PI3K-Akt signaling pathways. Moreover, the hub genes, including ITGA5, ITGB3, ITGA2, LAMC2, MMP2, and ITGA4, might contribute to SMV-induced pulmonary toxicity. Our study improves the understanding of the molecular mechanisms by which SMV induced the pulmonary toxicity.

摘要

钒暴露对人体肺功能有不良影响,而钒暴露诱导的肺毒性的详细机制有限。因此,本研究旨在探讨与五氧化二钒(SMV)诱导的肺毒性相关的枢纽基因和信号通路。从基因表达综合数据库(GEO)中下载的转录表达谱 GSE36684 包含 8 个人支气管上皮细胞(HBEC)样本,包括 5 个 SMV 处理组和 3 个对照组 HBEC 样本。共筛选出 455 个差异表达基因(DEGs),其中 SMV 处理的 HBEC 中分别有 201 个和 254 个基因上调和下调。基因本体论分析表明,DEGs 主要参与信号转导、药物反应、细胞增殖、黏附和迁移。通路分析表明,DEGs 主要参与 NF-κB、Wnt、MAPK 和 PI3K-Akt 信号通路。此外,ITGA5、ITGB3、ITGA2、LAMC2、MMP2 和 ITGA4 等枢纽基因可能有助于 SMV 诱导的肺毒性。本研究提高了对 SMV 诱导肺毒性的分子机制的认识。

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