西亚试剂：Bald scalp in men with androgenetic alopecia retains hair f

Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells

Luis A. Garza1, Chao-Chun Yang2,3, Tailun Zhao1, Hanz B. Blatt1, Michelle Lee1, Helen He1, David C. Stanton4, Lee Carrasco4, Jeffrey H. Spiegel5, John W. Tobias6 and George Cotsarelis1

1Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

2Department of Dermatology and

3Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

4Department of Oral and Maxillofacial Surgery, University of Pennsylvania School of Dental Medicine and University of Pennsylvania Health System, Philadelphia, Pennsylvania, USA.

5Department of Plastic Surgery, Boston University, Boston, Massachusetts, USA.

6Penn Bioinformatics Core, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

Androgenetic alopecia (AGA), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from AGA individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15hi stem cells were maintained in bald scalp samples. However, CD200hiITGA6hi and CD34hi cell populations — which both possessed a progenitor phenotype, in that they localized closely to the stem cell–rich bulge area but were larger and more proliferative than the KRT15hi stem cells — were markedly diminished. In functional assays, analogous CD200hiItga6hi cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of AGA.

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