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骨形态发生蛋白信号传导通过限制上皮干细胞/祖细胞的激活和增殖来抑制毛囊生长期诱导。

Bone morphogenetic protein signaling inhibits hair follicle anagen induction by restricting epithelial stem/progenitor cell activation and expansion.

作者信息

Zhang Jiwang, He Xi C, Tong Wei-Gang, Johnson Teri, Wiedemann Leanne M, Mishina Yuji, Feng Jian Q, Li Linheng

机构信息

Stowers Institute for Medical Research, 1000 E 50th Street, Kansas City, Missouri 64110, USA.

出版信息

Stem Cells. 2006 Dec;24(12):2826-39. doi: 10.1634/stemcells.2005-0544. Epub 2006 Sep 7.

Abstract

Epithelial stem cells (EP-SCs) located in the bulge region of a hair follicle (HF) have the potential to give rise to hair follicle stem/progenitor cells that migrate down to regenerate HFs. Bone morphogenetic protein (BMP) signaling has been shown to regulate the HF cycle by inhibiting anagen induction. Here we show that active BMP signaling functions to prevent EP-SC activation and expansion. Dynamic expression of Noggin, a BMP antagonist, releases EP-SCs from BMP-mediated restriction, leading to EP-SC activation and initiation of the anagen phase. Experimentally induced conditional inactivation of the BMP type IA receptor (Bmpr1a) in EP-SCs leads to overproduction of HF stem/progenitor cells and the eventual formation of matricomas. This genetic manipulation of the BMP signaling pathway also reveals unexpected activation of beta-catenin, a major mediator of Wnt signaling. We propose that BMP activity controls the HF cycle by antagonizing Wnt/beta-catenin activity. This is at least partially achieved by BMP-mediated enhancement of transforming growth factor-beta-regulated epithelial cell-specific phosphatase (PTEN) function. Subsequently, PTEN, through phosphatidyl inositol 3-kinase-Akt, inhibits the activity of beta-catenin, the convergence point of the BMP and Wnt signaling pathways.

摘要

位于毛囊(HF)隆突区的上皮干细胞(EP-SCs)有潜力产生毛囊干细胞/祖细胞,这些细胞向下迁移以再生毛囊。骨形态发生蛋白(BMP)信号已被证明通过抑制生长期诱导来调节毛囊周期。在此我们表明,活跃的BMP信号发挥作用以阻止EP-SC的激活和扩增。BMP拮抗剂Noggin的动态表达使EP-SCs从BMP介导的限制中释放出来,导致EP-SC激活并启动生长期。实验性诱导EP-SCs中BMP IA型受体(Bmpr1a)的条件性失活会导致毛囊干细胞/祖细胞过度产生并最终形成基质瘤。对BMP信号通路的这种基因操作还揭示了Wnt信号的主要介导因子β-连环蛋白的意外激活。我们提出,BMP活性通过拮抗Wnt/β-连环蛋白活性来控制毛囊周期。这至少部分是通过BMP介导的转化生长因子-β调节的上皮细胞特异性磷酸酶(PTEN)功能增强来实现的。随后,PTEN通过磷脂酰肌醇3-激酶-Akt抑制β-连环蛋白的活性,β-连环蛋白是BMP和Wnt信号通路的交汇点。

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