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Reoccurrence of c<jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content> in high\u2010risk patients is prevented by oral retinoids. But oral retinoid treatment causes significant side effects; and patients develop retinoid resistance. Exactly how retinoids prevent <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010induced c<jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content> is currently not well understood. Retinoid resistance blocks mechanistic studies in the leading mouse model of c<jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content>, the <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010exposed <jats:styled-content style=\"fixed-case\">SKH<\/jats:styled-content>\u20101 hairless mouse. To begin to understand the role of retinoids in <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010induced c<jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content> we first examined the localization pattern of key retinoid metabolism proteins by immunohistochemistry 48\u00a0h after <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> treatment of female <jats:styled-content style=\"fixed-case\">SKH<\/jats:styled-content>\u20101 mice. We next inhibited retinoic acid (<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>) synthesis immediately after <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> exposure. Acute <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> increased <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content> synthesis, signaling and degradation proteins in the stratum granulosum. Some of these proteins changed their localization; while other proteins just increased in intensity. In contrast, acute <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> reduced the retinoid storage protein lectin:retinol acyltransferase (<jats:styled-content style=\"fixed-case\">LRAT<\/jats:styled-content>) in the epidermis. Inhibiting <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content> synthesis disrupted the epidermis and impaired differentiation. These data suggest that repair of the epidermis after acute <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> exposure requires endogenous <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content> synthesis.<\/jats:p>","DOI":"10.1111\/php.12441","type":"journal-article","created":{"date-parts":[[2015,2,26]],"date-time":"2015-02-26T07:07:38Z","timestamp":1424934458000},"page":"901-908","source":"Crossref","is-referenced-by-count":11,"title":["Endogenous Retinoic Acid Required to Maintain the Epidermis Following Ultraviolet Light Exposure in SKH\u20101 Hairless Mice"],"prefix":"10.1111","volume":"91","author":[{"given":"Katherine L.","family":"Gressel","sequence":"first","affiliation":[{"name":"Department of Human Sciences (Nutrition) the Ohio State University Columbus OH"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F. 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