Abstract

Vitiligo is the most commonly acquired depigmented disorder of the skin that is characterized by the destruction of melanocytes (MCs) resulting in achromic macules. Although narrow-band UVB (NB-UVB) has been clinically proven to be an effective therapeutic option in the treatment of vitiligo, the mechanism by which how NB-UVB induces repigmentation in vitiligo has not been clearly elucidated. In this study, we examined the role of P53/miR211/MMP9 in the migration of MCs upon NB-UVB exposure. The primary human epidermal MCs were cultured from human foreskin. The mRNA and protein levels of P53, TRPM1, and MMP9 were measured using qPCT and western blotting assay. Transwell ®-collagen IV-coated membrane inserts were used for measuring the MCs migration ability. The migration ability was also examined in the MCs transfected with hsa-mir211 mimic and lentivirus-P53 in the presence or absence of NB-UVB irradiation. The results showed that in NB-UVB-exposed MCs, there was a significant increase in P53 and MMP9 levels alongside a decrease in TRPM1 and miR211 levels. We also found that the migration ability and MMP9 level of MCs transfected with hsa-miR211 mimic or/ lentivirus-P53 were significantly changed as compared with controls. Collectively , our results indicate that the P53/miR211/MMP9 axis plays a critical role in facilitating the migration of MCs exposed to NB-UVB irradiation, which may serve as a provocative target for promoting vitiligo repigmentation. (This study was supported by grant from the National Natural Science Foundation of China, NSFC#: 81573028)

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