Effect of acute ultraviolet light B on retinoic acid and 3,4-didehydroretinoic acid synthesis in human skin equivalent
Ultraviolet light B (UVB)-damaged skin repairs itself spontaneously, while chronic UVB exposure results in squamous cell carcinoma (SCC). Oral retinoids prevent the reoccurrence of SCC. Retinoids include vitamin A1 (retinol), vitamin A2 (3,4- didehydroretinol/ddretinol), retinoic acid (RA), and 3,4-didehydroRA (ddRA). Cytochrome P450 27C1 (CYP27C1) catalyzes the formation of ddretinol from retinol. Dehydrogenase reductase SDR family member 9 (DHRS9) catalyzes the first step of the conversion of Retinol to RA in skin. DHRS9 increased following acute UVB irradiation, but decreased during progression to SCC in mice. Furthermore, inhibition of RA biosynthesis after acute UVB irradiation damaged the skin. To better understand how these genes contribute to epidermal repair, we created human skin equivalents (HSEs). These HSEs were exposed to 500 and 2500 J/m2 UVB. Samples were collected 24 hours later. We are measuring DHRS9 and CYP27C1 by quantitative polymerase chain reaction (QPCR). Our hypothesis is that these genes will increase.
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