表皮基底上层变异维甲酸X受体转基因鼠抑制表皮基层角朊细胞增殖

为了解维甲酸受体RXRα在活体表面角朊细胞增殖分化中的作用，对缺AF－2激活功能段的RXRα变异基因及仅在表皮基底上层表达的牛角蛋白10作为启动子的转基因鼠进行研究。发现鼠表皮发育无异常。以tRA、人工合成选择结合于RAR的CD367分别局部处理后，CRABPⅡ、CRBPⅠ、CRBPⅡmRNA的诱导表达明显低于正常鼠．表皮增厚及基层细胞有丝分裂也明显减少。而对人工合成选择结合于、RXR的SR11237无反应。说明体内表皮维甲酸受体以RARγ／RXRα条合双倍体形式为主；表皮基底上层细胞通过维甲酸细胞间信号传递可调控基层细胞的增殖。

SUPRABASAL RXR MUTANT IN TRANSGENIC MOUSE INHIBITS EPIDERMAL BASAL KERATINOCYTE PROLIFERATION

To determine the effects of RXRQ on keratinocytes proliferation in vivo, transgenic mice with a mutant of dominat-negative RXRQ lacking transactivation function AF-2 and a promotor of boine keratin lo which only expresses in suprabasal keratinocytes were investigated. No abnormal devel opment of the mice epidermis was found. Treated with tRA, synthetic selective-RAR CD367 respective-ly, the inductive expression of CRABP , CRBP I,and CRBP Ⅱ was obvious1y lower than that of the normal controls- Epidermal hyperplasia and basal cell initosis also decreased. No effects were de-tectable of synthetic selective-RXR SR11237. This suggests that heterdimers RARr/RXRQ are predom-inant in epidermis in vivo;suprabasal cell can regu-late basal cell,s proliferation via retinoic acid signal-ing pass way.