Photoprotection by 1α,25-dihydroxyvitamin D and analogs: Further studies on mechanisms and implications for UV-damage
Ultraviolet (UV) irradiation causes DNA damage in skin cells, immunosuppression and photocarcinogenesis. 1α,25-dihydroxyvitamin D3 (1,25D) reduces UV-induced DNA damage in the form of cyclobutane pyrimidine dimers (CPD) in human keratinocytes in culture and in mouse and human skin. UV-induced immuno...
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| Published in: | Journal of steroid biochemistry and molecular biology Vol. 121; no. 1; pp. 164 - 168 |
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| Format: | Journal Article Conference Proceeding |
| Language: | English |
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| Abstract | Ultraviolet (UV) irradiation causes DNA damage in skin cells, immunosuppression and photocarcinogenesis. 1α,25-dihydroxyvitamin D3 (1,25D) reduces UV-induced DNA damage in the form of cyclobutane pyrimidine dimers (CPD) in human keratinocytes in culture and in mouse and human skin. UV-induced immunosuppression is also reduced in mice by 1,25D, in part due to the reduction in CPD and a reduction in interleukin (IL-6. The
cis-locked analog, 1α,25-dihydroxylumisterol3 (JN), which has almost no transactivating activity, reduces UV-induced DNA damage, apoptosis and immunosuppression with similar potency to 1,25D, consistent with a non-genomic signalling mechanism. The mechanism of the reduction in DNA damage in the form of CPD is unclear. 1,25D doubles nuclear expression of p53 compared to UV alone, which suggests that 1,25D facilitates DNA repair. Yet expression of a key DNA repair gene,
XPG is not affected by 1,25D. Chemical production of CPD has been described. Incubation of keratinocytes with a nitric oxide donor, SNP, induces CPD in the dark. We previously reported that 1,25D reduced UV-induced nitrite in keratinocytes, similar to aminoguanidine, an inhibitor of nitric oxide synthase. A reduction in reactive nitrogen species has been shown to facilitate DNA repair, but in view of these findings may also reduce CPD formation via a novel mechanism. |
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| AbstractList | Ultraviolet (UV) irradiation causes DNA damage in skin cells, immunosuppression and photocarcinogenesis. 1α,25-dihydroxyvitamin D3 (1,25D) reduces UV-induced DNA damage in the form of cyclobutane pyrimidine dimers (CPD) in human keratinocytes in culture and in mouse and human skin. UV-induced immunosuppression is also reduced in mice by 1,25D, in part due to the reduction in CPD and a reduction in interleukin (IL-6. The
cis-locked analog, 1α,25-dihydroxylumisterol3 (JN), which has almost no transactivating activity, reduces UV-induced DNA damage, apoptosis and immunosuppression with similar potency to 1,25D, consistent with a non-genomic signalling mechanism. The mechanism of the reduction in DNA damage in the form of CPD is unclear. 1,25D doubles nuclear expression of p53 compared to UV alone, which suggests that 1,25D facilitates DNA repair. Yet expression of a key DNA repair gene,
XPG is not affected by 1,25D. Chemical production of CPD has been described. Incubation of keratinocytes with a nitric oxide donor, SNP, induces CPD in the dark. We previously reported that 1,25D reduced UV-induced nitrite in keratinocytes, similar to aminoguanidine, an inhibitor of nitric oxide synthase. A reduction in reactive nitrogen species has been shown to facilitate DNA repair, but in view of these findings may also reduce CPD formation via a novel mechanism. |
| Author | Mason, R.S. Dilley, A. Halliday, G.M. Gordon-Thomson, C. Sequeira, V.B. Norman, A.W. Dixon, K.M. Feldman, D. Pobre, K. Mizwicki, M.T. Reeve, V.E. |
| Author_xml | – sequence: 1 givenname: R.S. surname: Mason fullname: Mason, R.S. email: rebeccam@physiol.usyd.edu.au organization: Dept of Physiology, Bosch Institute, Anderson Stuart Bldg F13, University of Sydney, NSW 2006, Australia – sequence: 2 givenname: V.B. surname: Sequeira fullname: Sequeira, V.B. organization: Dept of Physiology, Bosch Institute, Anderson Stuart Bldg F13, University of Sydney, NSW 2006, Australia – sequence: 3 givenname: K.M. surname: Dixon fullname: Dixon, K.M. organization: Dept of Physiology, Bosch Institute, Anderson Stuart Bldg F13, University of Sydney, NSW 2006, Australia – sequence: 4 givenname: C. surname: Gordon-Thomson fullname: Gordon-Thomson, C. organization: Dept of Physiology, Bosch Institute, Anderson Stuart Bldg F13, University of Sydney, NSW 2006, Australia – sequence: 5 givenname: K. surname: Pobre fullname: Pobre, K. organization: Dept of Physiology, Bosch Institute, Anderson Stuart Bldg F13, University of Sydney, NSW 2006, Australia – sequence: 6 givenname: A. surname: Dilley fullname: Dilley, A. organization: 352 President Ave, Gymea, NSW 2227, Australia – sequence: 7 givenname: M.T. surname: Mizwicki fullname: Mizwicki, M.T. organization: Dept of Biochemistry, 5456 Boyce Hall, University of California, Riverside, CA 92521-0129, USA – sequence: 8 givenname: A.W. surname: Norman fullname: Norman, A.W. organization: Dept of Biochemistry, 5456 Boyce Hall, University of California, Riverside, CA 92521-0129, USA – sequence: 9 givenname: D. surname: Feldman fullname: Feldman, D. organization: Dept of Medicine, Division of Endocrinology, Stanford University School of Medicine, 300 Pasteur Drive, Room S-025, Stanford, CA 94305-5103, USA – sequence: 10 givenname: G.M. surname: Halliday fullname: Halliday, G.M. organization: Dept of Medicine, Bosch Institute, Blackburn Bldg D06, University of Sydney, Sydney, NSW 2006, Australia – sequence: 11 givenname: V.E. surname: Reeve fullname: Reeve, V.E. organization: Faculty of Veterinary Science, McMaster Bldg B14, University of Sydney, Sydney, NSW 2006, Australia |
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| Keywords | Ultraviolet radiation 1α,25-Dihydroxyvitamin D3 Photoprotection Cancer Malignant tumor Analog |
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| Title | Photoprotection by 1α,25-dihydroxyvitamin D and analogs: Further studies on mechanisms and implications for UV-damage |
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