Role of androgen in mesenchymal epithelial interactions in human hair follicle

Role of androgen in mesenchymal epithelial interactions in human hair follicle
复制标题

DOI:
10.1111/j.1087-0024.2005.10107.x
复制
发表时间:
2005-12-01
影响因子:
--
通讯作者:
Inui, S
Inui, S
中科院分区:
其他
文献类型:
--
作者:
Itami, S;Inui, S

文献摘要

被引文献

相似文献

人类毛囊分布在身体的各个特定部位,似乎对雄激素依赖性生长具有遗传易感性。胡须、腋窝和前额头皮毛乳头细胞(DPC)最近被证明具有雄激素靶细胞的特性。这些DPC显示雄激素受体的强表达,并且II型5 α还原酶的表达仅限于胡须和额部头皮DPC。这些结果表明,DPC介导的雄激素信号的滤泡上皮细胞的旁分泌方式。我们开发了一个体外共培养系统,使用DPC和角质形成细胞(KC)的特点雄激素的作用模式在人类毛囊。雄激素能显著刺激与胡须DPC共培养的KC增殖,表明胡须DPC产生雄激素依赖性扩散生长因子。胰岛素样生长因子-I被鉴定为胡须DPC产生的雄激素依赖性旁分泌生长因子之一。我们还确定了雄激素对KC的生长的抑制作用与DPC从雄激素性脱发(阿加)的DPC与编码雄激素受体的表达载体转染。这种KC的生长抑制是由来自阿加DPC的转化生长因子-β 1(TGF-β 1)介导的,表明TGF-β 1是阿加的旁分泌介质。
Human hair follicles, which are distributed in various and specific sites of the body, appear to have an inherited susceptibility for androgen-dependent growth. Beard, axillary, and frontal scalp dermal papilla cells (DPC) were recently shown to possess the characteristics of androgen target cells. These DPC show strong expression of androgen receptors, and the expression of type II 5 alpha reductase is restricted to beard and frontal scalp DPC. These findings suggest that DPC mediate the signals of androgen to follicular epithelial cells in a paracrine fashion. We developed an in vitro co-culture system using DPC and keratinocytes (KC) to characterize the mode of androgen action in human hair follicles. Androgen significantly stimulated the proliferation of KC co-cultured with beard DPC, indicating that beard DPC produce androgen-dependent diffusible growth factors. Insulin-like growth factor-I was identified as one of the androgen-dependent paracrine growth factors produced by beard DPC. We also identified the inhibitory role of androgen on the growth of KC co-cultured with DPC from androgenetic alopecia (AGA) when the DPC were transfected with an expression vector encoding the androgen receptor. This growth suppression of KC was mediated by transforming growth factor-beta 1 (TGF-beta 1) derived from DPC of AGA, suggesting that TGF-beta 1 is a paracrine mediator for AGA.