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Ergocalciferol promotes in vivo differentiation of keratinocytes and reduces photodamage caused by ultraviolet irradiation in hairless mice
Author(s) -
Mitani Hiroaki,
Naru Eiji,
Yamashita Mika,
Arakane Kumi,
Suzuki Tadashi,
Imanari Toshio
Publication year - 2004
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/j.1600-0781.2004.00116.x
Subject(s) - hairless , vitamin d and neurology , ergocalciferol , epidermis (zoology) , chemistry , in vivo , human skin , keratinocyte , pharmacology , endocrinology , medicine , cholecalciferol , biology , in vitro , biochemistry , anatomy , genetics , microbiology and biotechnology
Background: Ergocalciferol (VD 2 ) is usually administered orally and it is metabolized to produce its biologically active metabolites in the liver and kidney. Active vitamin D is a well‐known potent regulator of cell growth and differentiation. Purpose: Active vitamin D such as 1,25‐dihydroxyvitamin D 3 (1α,25(OH) 2 D 3 ) prevents photodamage, including wrinkles and morphologic alterations. However, its clinical and cosmetic use is limited because of its potent, associated effect on calcium metabolism. We examined the efficacy of vitamin D analogues with few adverse effects for preventing skin photodamage. Method: Topical application of VD 2 to hairless mouse dorsal skin, and exposure to solar‐simulating ultraviolet (UV) radiation at a dose of 10.8 J/cm 2 (UVA) were performed for 15 weeks, five times a week on weekdays. At the end of the final irradiation, histological and analytical studies were performed. Results: Topical application of VD 2 significantly prevented wrinkle formation and abnormal accumulation of extracellular matrix components. In addition, VD 2 suppressed excessive secretion of IL‐6 induced by UV irradiation in cultured human normal keratinocytes, in a dose‐dependent manner. Conclusion: VD 2 promoted keratinocytes differentiation in the epidermis and showed diverse physiological effects, the same as the active form of VD 3 . The results suggested that the suppression of skin photodamage involved the promotion of keratinocytes differentiation and suppression of IL‐6 secretion induced by exposure to UV. Topical application of VD 2 may become an effective means to suppress solar UV‐induced human skin damage.