ArticleMolecular and cellular biochemistry2012
UVA/B exposure promotes the biosynthesis of dehydroretinol in cultured human keratinocytes.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- 3,4-Desaturation of retinoic acid by cytochrome P450 27C1 prevents P450-mediated catabolism.Archives of biochemistry and biophysics · 2023Article
- Retinoids in Cutaneous Squamous Cell Carcinoma.Nutrients · 2021Review
- Human cytochrome P450 enzymes 5-51 as targets of drugs and natural and environmental compounds: mechanisms, induction, and inhibition - toxic effects and benefits.Drug metabolism reviews · 2018Review
- Human mitochondrial cytochrome P450 27C1 is localized in skin and preferentially desaturatesThe Journal of biological chemistry · 2017Article
- Melanoma Chemoprevention: Current Status and Future Prospects.Photochemistry and photobiology · 2017Review
- Human cytochrome P450 27C1 catalyzes 3,4-desaturation of retinoids.FEBS letters · 2016Article
- Endogenous Retinoic Acid Required to Maintain the Epidermis Following Ultraviolet Light Exposure in SKH-1 Hairless Mice.Photochemistry and photobiologyArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinol and its metabolites modulate epithelial differentiation and serve as cellular UV sensors through changes in retinoid status. Of note is the dehydroretinol family which may serve functions distinct from parental retinol. This study focuses on the metabolism of this family and its potential participation in the response of normal epidermal human keratinocytes to UV irradiation. There were three findings. First, keratinocytes contain two pools of dehydroretinyl esters, one of which is shielded from UVB-, but not from UVA-induced decomposition. Second, using a novel in vitro assay we demonstrated that both UVA and UVB promote dehydroretinol biosynthesis in keratinocytes, but only UVB exposure promotes retinoid ester accretion by enhancing the activity of at least one acyl transferase. Finally, dehydroretinol sufficiency reduces UVA/B driven apoptosis more effectively than retinol sufficiency. This may in part be due to differences in the expression of Fas ligand, which we found to be upregulated by retinoic acid, but not dehydroretinoic acid. These observations implicate a role of dehydroretinol and its metabolites in UVA/B adaptation. Thus, the keratinocyte response to UV is jointly shaped by both the retinoids and dehydroretinoids.
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Registered trials
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