BioAcyl Corp
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Hong, S. P., Kim, M. J., & Jung, M.-Y. (2008). Biopositive Effects of Low-Dose UVB on Epidermis: Coordinate Upregulation of Antimicrobial Peptides and Permeability Barrier Reinforcement. Journal of Investigative Dermatology, 128(12), 2880–2887. Added by: Dr. Enrique Feoli (04/12/2023, 18:10) Last edited by: Dr. Enrique Feoli (04/12/2023, 18:25) |
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| Resource type: Journal Article DOI: 10.1038/jid.2008.169 ID no. (ISBN etc.): 0022-202X, 1523-1747 BibTeX citation key: Hong2008 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: UV Damage Repair Creators: Hong, Jung, Kim Collection: Journal of Investigative Dermatology |
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| Abstract |
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Whereas high-dose ultraviolet B (UVB) is detrimental to the epidermal permeability barrier, suberythemal doses of UVB are used to treat atopic dermatitis (AD), which is characterized by defective permeability barrier and antimicrobial function. As epidermal permeability barrier and antimicrobial peptide (AMP) expression are coregulated and interdependent functions, we hypothesized that suberythemal doses of UVB exposure could regulate AMP expression in parallel with permeability barrier function. Hairless mice were exposed to 40 mJ cm−2 UVB (about 1/2 minimal erythema dose) daily for 1 or 3 days. Twenty-four hours after the last exposure, epidermal barrier function was assessed and skin specimens were taken for western blotting, immunohistochemistry, and quantitative reverse transcription-PCR for mouse β-defensin (mBD)-2, mBD3 and cathelin-related antimicrobial peptide (CRAMP). mRNA levels of the vitamin D receptor (VDR), 1α-hydroxylase and key epidermal lipid synthetic enzymes were also quantified. After 3 days of UVB exposure, acceleration of barrier recovery and augmentation in expression of epidermal differentiation markers (for example, involucrin and filaggrin) occurred in parallel with increased mBD2, mBD3, and CRAMP expression at both the mRNA and protein level. VDR, 1α-hydroxylase, and the major epidermal lipid synthetic enzymes were also upregulated. When an inhibitor of 1α, 25 dihydroxyvitamin D3 formation, ketoconazole, was applied immediately after UVB exposure, the cutaneous vitamin D system was inhibited, which in turn blocked epidermal lipid synthesis, AMP expression, and permeability barrier homeostasis, suggesting that the beneficial effect of low-dose UVB depends, at least in part, on activation of the cutaneous vitamin D system. Our results provide new insights into the mechanisms whereby low-dose UVB comprises effective therapy for AD.
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| Notes |
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The evolution of DarkPigmentation would have provided important benefits: first and foremost, it would have “reset” the threshold for UV-B-induced toxicity, while simultaneously providing the additional, substantial benefits of “suberythemogenic” UV-B.
https://onlinelibrary.wiley.com/doi/10.1111/eva.12858 Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |