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Suppression of proliferation of human epidermal keratinocytes by 1,25‐dihydroxyvitamin D 3 Analysis of its effect on psoriatic lesion and of its mechanism using human keratinocytes in culture
Author(s) -
KITANO Y.,
IKEDA N.,
OKANO M.
Publication year - 1991
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1991.tb01358.x
Subject(s) - psoriasis , keratinocyte , cell cycle , lesion , flow cytometry , cell growth , human skin , mitosis , cell culture , cell , in vitro , cancer research , chemistry , biology , medicine , pathology , endocrinology , microbiology and biotechnology , immunology , biochemistry , genetics
. Psoriasis is a genetically determined chronic disease of the skin, and an accelerated proliferation of epidermal keratinocytes is one of the pathophysiological characteristics of psoriatic lesion. Recently, it was reported that topical administration of 1,25‐dihydroxyvitamin D 3 was effective for psoriasis. Our study was done to investigate the effect of 1,25‐(OH) 2 ‐D 3 on cell kinetics on human epidermal keratinocytes as a possible mechanism of its effect on psoriasis. After 24‐h application of 1 μg g –1 1,25‐(OH) 2 ‐D 3 ointment to psoriatic lesion, the number of mitotic keratinocytes decreased. When the cultured human keratinocytes were exposed to 10 –8 mol l –1 1,25‐(OH) 2 ‐D 3 for more than 9 days, inhibition of cell proliferation was noted. DNA distribution analysis by flow cytometry showed a decrease in cells in the S phase, and increase in 2c cells. This indicates blockade of the cell cycle in the G 1 phase. The cell cycle time was not extended as a result of 1,25‐(OH) 2 ‐D 3 ‐treatment.