Obinata A, Kawada M, Endo H
Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan.
Endocrinol Jpn. 1990 Jun;37(3):463-9. doi: 10.1507/endocrj1954.37.463.
When undifferentiated skin from 13-day-old chick embryos was cultured in a chemically defined medium, glucocorticoid specifically decreased the dexamethasone-binding activity of the epidermal cytosol after 1 day of culture, 3 days before it induced formation of a cornified layer over the intermediate cells of the epidermis. The binding activity reappeared after removal of the steroid from the medium. This reappearance was inhibited by epidermal growth factor (EGF, 100 ng/ml). The Addition of 2 microM retinol resulted in a 3-fold increase in specific dexamethasone binding in the epidermal cytosol within 12 h with no change in the binding affinity. The inhibition of glucocorticoid-induced keratinization by retinol is due a to mechanism other than inactivation of the glucocorticoid receptor.
当将13日龄鸡胚的未分化皮肤在化学成分明确的培养基中培养时，糖皮质激素在培养1天后特异性降低了表皮细胞质溶胶的地塞米松结合活性，这比它诱导表皮中间细胞上形成角质化层提前3天。从培养基中去除类固醇后，结合活性重新出现。表皮生长因子（EGF，100 ng/ml）可抑制这种重新出现。添加2 microM视黄醇在12小时内使表皮细胞质溶胶中的特异性地塞米松结合增加了3倍，而结合亲和力没有变化。视黄醇对糖皮质激素诱导的角质化的抑制作用是由于一种不同于糖皮质激素受体失活的机制。
