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• W2897958602 abstract "Abstract Oxidative stress leads to melanocyte death and has been implicated in the pathogenesis of vitiligo. The nuclear factor, E2‐related factor 2 (Nrf2), is a critical transcription factor in protecting cells from oxidative damage. High‐mobility group box 1 ( HMGB 1) is a chromatin‐associated nuclear protein and an extracellular damage‐associated molecular pattern molecule. Extracellular HMGB 1 released from activated immune cells, necrotic or injured cells, becomes a proinflammatory mediator through binding to cell‐surface receptors of responding cells. In this study, we investigated the role of HMGB 1 from melanocytes in the response to oxidative stress and the mechanism involved. We showed that HMGB 1 is expressed by primary normal human epidermal melanocytes ( NHEM s). H 2 O 2 treatment increased cytoplasmic translocation and extracellular release of HMGB 1. HMGB 1 knockdown by small interfering RNA (si RNA ) led to decreased apoptosis of NHEM s. HMGB 1 inhibition enhanced the expression of Nrf2 and its target genes. The expression of Nrf2 and its downstream antioxidant genes was downregulated after the supernatant of H 2 O 2 ‐treated NHEM s was added to HMGB 1‐deficient cells. HMGB 1 knockdown by si RNA suppressed the expression of the autophagosome marker, LC 3, and enhanced p62 expression. Coimmunoprecipitation with Keap1 showed a reduced Nrf2‐Keap1 interaction and an increased p62‐Keap1 interaction under oxidative stress. These data demonstrated that external stimuli (eg, oxidative stress) may trigger autocrine HMGB 1 translocation and release by melanocytes, suppressing the expression of Nrf2 and downstream antioxidant genes to induce melanocyte apoptosis, and thereby participate in the pathological process of vitiligo." @default.
• W2897958602 created "2018-10-26" @default.
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• W2897958602 date "2018-10-19" @default.
• W2897958602 modified "2023-10-01" @default.
• W2897958602 title "HMGB1 deficiency reduces H₂ O₂ -induced oxidative damage in human melanocytes via the Nrf2 pathway" @default.
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• W2897958602 doi "https://doi.org/10.1111/jcmm.13895" @default.
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