EFFECT OF I.2 MMOL/1 CALCIUM, TRIAMCINOLONE ACETONIDE, AND RETINOIDS ON LOW-CALCIUM REGULATED KERATINOCYTE DIFFERENTIATION
EFFECT OF I.2 MMOL/1 CALCIUM, TRIAMCINOLONE ACETONIDE, AND RETINOIDS ON LOW-CALCIUM REGULATED KERATINOCYTE DIFFERENTIATION
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DOI：
10.1111/j.1365-2133.1984.tb15583.x
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发表时间：
1984-01-01
影响因子：
10.3
通讯作者：
FAIRLEY, JA
中科院分区：
文献类型：
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作者：
MARCELO, CL;GOLD, RC;FAIRLEY, JA
新生小鼠角质形成细胞在低钙(001 mmoL/l)培养条件下生长迅速，与正常1.2 mmo1/l钙培养的细胞相比，生长速度快，层积少。研究了低钙对角质形成细胞特异性分化蛋白合成和数量的影响，以及10-8mol/l曲安奈德、6/μg/ml维甲酸和依维甲酸酯(RO10-9359)对低钙调节的角质形成细胞过度增殖和分化的影响。与正常钙调节的角质形成细胞相比，低钙调节的角质形成细胞含有更少的非共价交联和二硫键交联的角蛋白，更少的细胞膜，更多的可溶于十二烷基硫酸钠的活细胞蛋白，以及略多的角质形成颗粒相关蛋白。切换到1.2 mm o l/l钙的培养24 h不影响这些蛋白质的量和合成。维甲酸和曲安奈德对低钙调节的角质形成细胞的增殖均有约50%的抑制作用。低钙细胞在这些药物中生长9天后，角蛋白和细胞膜蛋白的含量都增加。我们的结论是，钙依赖过程可以调节表皮角质形成细胞的增殖和分化。我们的研究表明，这些钙调节事件可能通过钙依赖蛋白的变化而发生。
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 10‐8mol/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.