Endogenous Retinoic Acid Required to Maintain the Epidermis Following Ultraviolet Light Exposure in SKH-1 Hairless Mice‡
| Autor: | Krista M. D. La Perle, Helen B. Everts, Tatiana M. Oberyszyn, Katherine Lynne Gressel, F. Jason Duncan |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Ultraviolet Rays
medicine.drug_class Stratum granulosum Retinoic acid Tretinoin Biology Biochemistry Article Mice chemistry.chemical_compound Ultraviolet light medicine Animals Retinoid Physical and Theoretical Chemistry skin and connective tissue diseases Mice Hairless Epidermis (botany) integumentary system Retinol General Medicine Hairless medicine.anatomical_structure chemistry Cancer research Female Epidermis medicine.drug |
| Popis: | Ultraviolet light B (UVB) exposure induces cutaneous squamous cell carcinoma (cSCC), one of the most prevalent human cancers. Reoccurrence of cSCC 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 cSCC is currently not well understood. Retinoid resistance blocks mechanistic studies in the leading mouse model of cSCC, the UVB exposed SKH-1 hairless mouse. To begin to understand the role of retinoids in UVB-induced cSCC we first examined the localization pattern of key retinoid metabolism proteins by immunohistochemistry 48 hours 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 suggests that repair of the epidermis after acute UVB exposure requires endogenous RA synthesis. |
| Databáze: | OpenAIRE |
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