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Effect of 1–2 mmol/1 calcium, triamcinolone acetonide, and retinoids on low‐calcium regulated keratinocyte differentiation
Author(s) -
MARCELO CYNTHIA L.,
GOLD R. C.,
FAIRLEY JANET A.
Publication year - 1984
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1984.tb15583.x
Subject(s) - calcium , keratinocyte , keratin , chemistry , retinoic acid , mole , triamcinolone acetonide , etretinate , cell growth , cellular differentiation , biochemistry , endocrinology , microbiology and biotechnology , in vitro , biology , immunology , psoriasis , paleontology , organic chemistry , gene
SUMMARY Neonatal mouse keratinocytes cultured in low calcium (001 mmol/1) show rapid growth and little stratification when compared with cells grown in normal 1·2 mmol/1 calcium. The effect of low calcium on the amount and synthesis of specific differentiation proteins was studied; additionally, the effect of 10 ‐8 mol/1 triamcinolone acetonide, and 6 /μg/ml of retinoic acid and of etretinate (Ro 10–9359) on low‐calcium regulated keratinocyte hyperproliferation and differentiation was determined. Low‐calcium regulated keratinocytes contained less non‐covalently cross‐linked and disulphide cross‐linked keratins, less cell envelopes, much greater amounts of SDS‐soluble viable cell proteins, and slightly more keratohyaline granule‐related proteins than normal‐calcium regulated keratinocytes. A 24 h switching time to 1·2 mmol/1 calcium medium did not affect the amounts or synthesis of these proteins. Both retinoids and triamcinolone acetonide inhibited by approximately 50% the proliferation of the low‐calcium regulated keratinocytes. Growth of low‐calcium cells in these drugs for 9 days increased the amounts of both keratins and cell envelope proteins in the cultures. We concluded that calcium‐dependent processes can regulate epidermal keratinocyte proliferation and differentiation. Our studies suggest that these calcium‐regulated events may occur via changes in calcium‐dependent proteins.