McGuire J, Langdon R, Birchall N, Kupper T
Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut 06510.
Ann N Y Acad Sci. 1988;548:283-90. doi: 10.1111/j.1749-6632.1988.tb18816.x.
Keratinocytes in culture produce detectable amounts of IL-1 alpha mRNA constitutively and can be stimulated to express increased amounts of IL-1 alpha mRNA by cycloheximide, PMA, and retinoic acid. Dexamethasone decreases the amount of IL-1 mRNA induced by these agents, as well as constitutive IL-1 alpha mRNA. RU 486, which interferes with glucocorticosteroid-receptor binding, decreases inhibition of TPA stimulation of IL-1 alpha mRNA by dexamethasone, which suggests that the inhibition by dexamethasone is through a conventional ligand-receptor mechanism.
培养中的角质形成细胞组成性地产生可检测量的IL-1α mRNA,并且可以被放线菌酮、佛波酯和视黄酸刺激以表达增加量的IL-1α mRNA。地塞米松减少这些试剂诱导的IL-1 mRNA量以及组成性IL-1α mRNA。RU 486干扰糖皮质激素受体结合,减少地塞米松对佛波酯刺激IL-1α mRNA的抑制,这表明地塞米松的抑制作用是通过传统的配体-受体机制。