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Assessing the potential molecular mechanism of arsenite-induced skin cell senescence. | LitMetric

Assessing the potential molecular mechanism of arsenite-induced skin cell senescence.

Toxicol Res (Camb)

Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education & School of Public Health, Guizhou Medical University, Dongqing Road 2, Guiyang 550025, China.

Published: October 2023

AI Article Synopsis

Article Abstract

Arsenic exposure is a public health concern worldwide. Skin damage, as a typical lesion of arsenic exposure, the mechanism is still unknown. Studies have found that cellular senescence plays a key role in arsenic-induced skin damage, and the previous research found that the ERK/CEBPB signaling pathway may be an important molecular event of arsenic-induced skin cell senescence, but its specific mechanism is unknown. In this study, genetic engineering technology was used to construct stable HaCaT cell lines, and the role and mechanism of ERK/CEBPB signaling pathway in arsenic-induced HaCaT cell senescence were verified by knockdown and overexpression of ERK and CEBPB in both forward and backward. It was found that knockdown of CEBPB or ERK can downregulate the ERK/CEBPB signaling pathway and reduce arsenic-induced skin cell senescence. In contrast to knockdown, overexpression of CEBPB or ERK can upregulate the ERK/CEBPB signaling pathway and aggravate the senescence of skin cells caused by arsenic. These findings suggest that sodium arsenite can further promote SASP secretion and the expression of p53, p21 and p16 by activating the ERK/CEBPB signaling pathway, induce cell cycle arrest and trigger cellular senescence.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615813PMC
http://dx.doi.org/10.1093/toxres/tfad075DOI Listing

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