In vivo relevance for photoprotection by the vitamin D rapid response pathway

Vitamin D is produced by exposure of 7-dehydrocholesterol in the skin to UV irradiation (UVR) and further converted in the skin to the biologically active metabolite, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and other compounds. UVR also results in DNA damage producing cyclobutane pyrimidine dimers (C...

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Bibliographic Details
Published in:Journal of steroid biochemistry and molecular biology 2007-03, Vol.103 (3-5), p.451-456
Main Authors: Dixon, K.M., Deo, S.S., Norman, A.W., Bishop, J.E., Halliday, G.M., Reeve, V.E., Mason, R.S.
Format: Article
Language:English
Subjects:
1,25-Dihydroxyvitamin D3
Biological and medical sciences
Cells, Cultured
Cyclobutane pyrimidine dimers (CPD)
Enzymes. Coenzymes. Vitamins. Pigments
Fundamental and applied biological sciences. Psychology
Humans
Immunosuppression
Metabolisms and neurohumoral controls
Molecular Structure
Signal Transduction - drug effects
Signal Transduction - radiation effects
Skh:hr1 hairless mice
Skin - drug effects
Skin - metabolism
Skin - radiation effects
Sunburn cells
Ultraviolet radiation
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Vitamin D
Vitamin D - analogs & derivatives
Vitamin D - chemistry
Vitamin D - pharmacology
Vitamin D analogs
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Summary:Vitamin D is produced by exposure of 7-dehydrocholesterol in the skin to UV irradiation (UVR) and further converted in the skin to the biologically active metabolite, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and other compounds. UVR also results in DNA damage producing cyclobutane pyrimidine dimers (CPD). We previously reported that 1,25(OH)2D3 at picomolar concentrations, protects human skin cells from UVR-induced apoptosis, and decreases CPD in surviving cells. 1,25(OH)2D3 has been shown to generate biological responses via two pathways—the classical steroid receptor/genomic pathway or a rapid, non-genomic pathway mediated by a putative membrane receptor. Whether the rapid response pathway is physiologically relevant is unclear. A cis-locked, rapid-acting agonist 1,25(OH)2lumisterol3 (JN), entirely mimicked the actions of 1,25(OH)2D3 to reduce fibroblast and keratinocyte loss and CPD damage after UVR. The effects of 1,25(OH)2D3 were abolished by a rapid-acting antagonist, but not by a genomic antagonist. Skh:hr1 mice exposed to three times the minimal erythemal dose of solar-simulated UVR and treated topically with 1,25(OH)2D3 or JN immediately after UVR showed reduction in UVR-induced UVR-induced sunburn cells (p
ISSN:0960-0760
1879-1220
DOI:10.1016/j.jsbmb.2006.11.016