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.
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