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While <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2\u2010regulated antioxidants are reported to protect melanocytes from oxidative stress, the role of <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 in the melanocyte response to monobenzone, a clinically relevant <jats:styled-content style=\"fixed-case\">VIP<\/jats:styled-content>, has not been characterised. We hypothesised that activation of <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 may protect melanocytes from monobenzone\u2010induced toxicity. We observed that knockdown of <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 or <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2\u2010regulated antioxidants <jats:styled-content style=\"fixed-case\">NQO<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">PRDX<\/jats:styled-content>6 reduced melanocyte viability, but not viability of keratinocytes and fibroblasts, suggesting that melanocytes were preferentially dependent upon <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 activity for growth compared to other cutaneous cells. Furthermore, melanocytes activated the <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 response following monobenzone exposure and constitutive <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 activation reduced monobenzone toxicity, supporting <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2's role in the melanocyte stress response. In contrast, melanocytes from individuals with vitiligo (vitiligo melanocytes) did not activate the <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 response as efficiently. Dimethyl fumarate\u2010mediated <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 activation protected normal and vitiligo melanocytes against monobenzone\u2010induced toxicity. Given the contribution of oxidant\u2010antioxidant imbalance in vitiligo, modulation of this pathway may be of therapeutic interest.<\/jats:p>","DOI":"10.1111\/exd.13350","type":"journal-article","created":{"date-parts":[[2017,3,31]],"date-time":"2017-03-31T07:25:30Z","timestamp":1490945130000},"page":"637-644","source":"Crossref","is-referenced-by-count":31,"title":["The nuclear factor (erythroid\u2010derived 2)\u2010like 2 (<scp>NRF<\/scp>2) antioxidant response promotes melanocyte viability and reduces toxicity of the vitiligo\u2010inducing phenol monobenzone"],"prefix":"10.1111","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5816-2270","authenticated-orcid":false,"given":"Omotayo A.","family":"Arowojolu","sequence":"first","affiliation":[{"name":"The Ronald O. 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