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Endogenous Retinoic Acid Required to Maintain the Epidermis Following Ultraviolet Light Exposure in SKH‐1 Hairless Mice
Author(s) -
Gressel Katherine L.,
Duncan F. Jason,
Oberyszyn Tatiana M.,
La Perle Krista M.,
Everts Helen B.
Publication year - 2015
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12441
Subject(s) - retinoid , hairless , epidermis (zoology) , retinoic acid , endogeny , cancer research , biology , downregulation and upregulation , microbiology and biotechnology , biochemistry , anatomy , gene
Ultraviolet light B ( UVB ) exposure induces cutaneous squamous cell carcinoma (c SCC ), one of the most prevalent human cancers. Reoccurrence of c SCC in high‐risk patients is prevented by oral retinoids. But oral retinoid treatment causes significant side effects; and patients develop retinoid resistance. Exactly how retinoids prevent UVB ‐induced c SCC is currently not well understood. Retinoid resistance blocks mechanistic studies in the leading mouse model of c SCC , the UVB ‐exposed SKH ‐1 hairless mouse. To begin to understand the role of retinoids in UVB ‐induced c SCC we first examined the localization pattern of key retinoid metabolism proteins by immunohistochemistry 48 h after UVB treatment of female SKH ‐1 mice. We next inhibited retinoic acid ( RA ) synthesis immediately after UVB exposure. Acute UVB increased RA 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 UVB reduced the retinoid storage protein lectin:retinol acyltransferase ( LRAT ) in the epidermis. Inhibiting RA synthesis disrupted the epidermis and impaired differentiation. These data suggest that repair of the epidermis after acute UVB exposure requires endogenous RA synthesis.