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首页> 外文期刊>Journal of dermatological science >Androgen receptor transactivity is potentiated by TGF-beta1 through Smad3 but checked by its coactivator Hic-5/ARA55 in balding dermal papilla cells.
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Androgen receptor transactivity is potentiated by TGF-beta1 through Smad3 but checked by its coactivator Hic-5/ARA55 in balding dermal papilla cells.

机译：TGF-beta1通过Smad3增强了雄激素受体的活性，但在脱毛的真皮乳头细胞中通过其辅助活化剂Hic-5 / ARA55对其进行了检查。

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摘要

We previously reported that TGF-beta1 is a paracrine mediator from dermal papilla to hair follicle epithelium in the pathogenesis of androgenetic alopecia (AGA) [1,2]. Because TGF-pi can induce catagen in hair cycling [3], it has been suggested that it functions as a paracrine pathogenic mediator from dermal papilla in AGA. On the other hand, TGF-betal reportedly modulates androgen receptor (AR) transactivation in the monkey kidney cell line CV-1 as well as the human prostate cell lines PC-3 and DU145 cells [4,5]. However, it depends on the cell type or conditions whether TGF-beta1 potentiates [5] or represses AR [4]. It is therefore ofconsiderable interest to examine potential modulation by TGF- beta1 and its downstream signaling for ARtranscriptional activity in balding dermal papilla cells (bald DPCs).
机译：我们先前曾报道，在雄激素性脱发（AGA）的发病机理中，TGF-beta1是从真皮乳头到毛囊上皮的旁分泌介质[1,2]。因为TGF-β1可以在毛发循环中诱导催化作用[3]，所以有人提出它可以作为AGA中真皮乳头的旁分泌致病介质。另一方面，据报道，TGF-β1调节猴肾细胞系CV-1以及人前列腺细胞系PC-3和DU145细胞中的雄激素受体（AR）反式激活[4,5]。但是，这取决于细胞类型或条件，TGF-beta1是否增强[5]或抑制AR [4]。因此，在秃顶的真皮乳头细胞（秃顶的DPC）中，研究TGF-β1的潜在调节及其下游信号转导AR转录活性具有极大的意义。

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