Lack of androgen receptor transcriptional activity in human keratinocytes
Lack of androgen receptor transcriptional activity in human keratinocytes
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DOI：
10.1016/s0923-1811(99)00091-2
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发表时间：
2000-06-01
影响因子：
4.6
通讯作者：
Chang, CS
中科院分区：
文献类型：
--
作者：
Inui, S;Itami, S;Chang, CS
由于检测雄激素受体（AR）在角质形成细胞的表达免疫染色是有争议的，我们研究了角质形成细胞是否可以作为雄激素的靶细胞使用瞬时转染试验。HaCaT角质形成细胞中内源性AR转录活性的氯霉素乙酰转移酶（CAT）测定表明，DHT（10（-9）-10（-8）M）可以诱导小于1.5倍的小鼠乳腺肿瘤病毒CAT，这是相当低的，相比之下，10（-7）M 1，25-二羟基维生素D-3对P450 cc 24-CAT的38倍诱导。AR共激活剂ARA 70或ARA 55不能增强这种低DHT介导的诱导。Western blotting分析表明HaCaT和正常角质形成细胞不表达AR蛋白。然而，外源性AR转染到HaCaT角质形成细胞中，可以安装AR转录活性，表明HaCaT角质形成细胞具有AR转录活性的所有必要的辅助因子。总之，角质形成细胞不太可能是雄激素的靶细胞。(C)2000爱思唯尔科学爱尔兰有限公司保留所有权利。
Since detection of androgen receptor (AR) expression in keratinocytes by immunostaining is controversial, we investigated whether keratinocytes can act as androgen target cells using transient transfection assays. Chloramphenicol acetyltransferase (CAT) assays for the endogenous AR transcriptional activity in HaCaT keratinocytes indicated that DHT (10(-9)-10(-8) M) can induce less than 1.5-fold of mouse mammary tumor virus CAT, which is quite low, compared with 38-fold induction by 10(-7) M 1,25-dihydroxyvitamin D-3 of P450cc24-CAT. Furthermore, this low DHT-mediated induction could not be enhanced by the AR co-activators, ARA70 or ARA55. Western blotting analysis indicated that HaCaT and normal keratinocytes do not express AR protein. Transfection of exogenous AR into HaCaT keratinocytes, however, could install AR transcriptional activity, suggesting that HaCaT keratinocytes have all the necessary accessory factors for AR transcription activity. In conclusion, keratinocytes are unlikely to be target cells for androgen. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.