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• W4211009968 abstract "Chronic exposure to high-dose inorganic arsenic through groundwater, air, or food remains a major environmental public health issue worldwide. Apoptosis, a method of cell death, has recently become a hot topic of research in biology and medicine. Previous studies have demonstrated that extracellular signal-regulated kinase (ERK) is related to arsenic-induced apoptosis. However, the reports are contradictory, and the knowledge of the above-mentioned mechanisms and their mutual regulation remains limited. In this study, the associations between the TGF-β1/ERK signaling pathway and arsenic-induced cell apoptosis were confirmed using the HaCaT cell model. The relative expressions of the indicators of the TGF-β1/ERK signaling pathway, apoptosis-related genes (cytochrome C, caspase-3, caspase-9, cleaved caspase-3, cleaved caspase-9, and Bax), the mitochondrial membrane potential, and the total apoptosis rate were significantly increased (P < .05), while the expression of the antiapoptosis gene Bcl-2 was significantly decreased (P < .05) in cells of the group exposed to arsenic. Moreover, the results demonstrated that the ERK inhibitor (PD98059) and TGF-β1 inhibitor (LY364947) could inhibit the activation of the ERK signaling pathway, thereby reducing the mitochondrial membrane potential, the total apoptosis rate, and the expression of pro-apoptosis-related genes in the cells, while the expression of the antiapoptosis gene Bcl-2 was significantly increased (P < .05). By contrast, the recombinant human TGF-β1 could promote apoptosis of the HaCaT cells by increasing the activation of the ERK signaling pathway (P < .05). These results indicate that inorganic arsenic promotes the apoptosis of human immortal keratinocytes through the TGF-β1/ERK signaling pathway." @default.
• W4211009968 created "2022-02-13" @default.
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• W4211009968 date "2022-02-10" @default.
• W4211009968 modified "2023-10-16" @default.
• W4211009968 title "Inorganic arsenic promotes apoptosis of human immortal keratinocytes through the <scp>TGF</scp> ‐β1/ <scp>ERK</scp> signaling pathway" @default.
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• W4211009968 doi "https://doi.org/10.1002/tox.23486" @default.
• W4211009968 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35142421" @default.
• W4211009968 hasPublicationYear "2022" @default.
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