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Originally published as MBC in Press, 10.1091/mbc.E08-07-0731 on December 10, 2008

Vol. 20, Issue 3, 882-890, February 1, 2009

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Disruption of Smad4 in Mouse Epidermis Leads to Depletion of Follicle Stem Cells

Leilei Yang, Lijuan Wang, and Xiao Yang

State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071, China

Submitted July 22, 2008; Revised November 21, 2008; Accepted December 2, 2008
Monitoring Editor: Jonathan Chernoff

Follicle stem cells (SCs) residing in the bulge region of a hair follicle (HF) can give rise to multiple lineages during the hair cycle and wound healing. The activation and self-renewal of follicle SCs must be tightly regulated to maintain the HF and epidermal homeostasis. Here we show that, in young mice, disruption of epidermal Smad4, the common mediator of transforming growth factor-β (TGF-β) signaling, stimulated the activation of follicle SCs, leading to hyperplasia of interfollicular epidermis (IFE), HFs, and sebaceous glands (SGs). Increased proliferation of follicle SCs ultimately exhausted the SC niche, indicated by the loss of bromodeoxyuridine (BrdU) label–retaining cells (LRCs), loss of keratin 15 (K15), and CD34 expression. In addition, the colony-forming efficiency of Smad4 mutant keratinocytes was significantly decreased. Increased nuclear localization of β-catenin and increased expression of c-Myc were correlated with the overactivation and depletion of follicle SCs. We concluded that Smad4 plays a pivotal role in follicle SC maintenance.

This was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E08-07-0731) on December 10, 2008.

Address correspondence to: Xiao Yang (yangx{at}nic.bmi.ac.cn)

Abbreviations used: BMP, bone morphogenetic protein; BMPR1A, BMP type 1a receptor; BrdU, bromodeoxyuridine; HF, hair follicle; IFE, interfollicular epidermis; K1, K14, and K15, keratin 1, 14, and 15, respectively; LRC, label-retaining cell; P20, postnatal day 20; SC, stem cell; SG, sebaceous gland; TGF-β, transforming growth factor-β.




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Y. Gao, G. Yang, T. Weng, J. Du, X. Wang, J. Zhou, S. Wang, and X. Yang
Disruption of Smad4 in Odontoblasts Causes Multiple Keratocystic Odontogenic Tumors and Tooth Malformation in Mice
Mol. Cell. Biol., November 1, 2009; 29(21): 5941 - 5951.
[Abstract] [Full Text] [PDF]


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