Androgenetic alopecia (AGA) is a frequent form of hair loss in both men and women. However, it is more common in men, in whom it is also known as male-pattern baldness. Through the analysis of bald and non-bald scalp samples from men with AGA, a team of researchers, led by George Cotsarelis, at the University of Pennsylvania School of Medicine, Philadelphia, has gained new insight into the underlying causes of AGA. Specifically, the data indicate that a defect in the conversion of hair follicle stem cells to progenitor cells has an important role in AGA. The authors therefore suggest that further studies defining the signals responsible for the transition of stem cells to progenitor cells could provide new therapeutic targets for the treatment of AGA.
TITLE: Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells
Source: Journal of Clinical Investigation
Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells
U.S. study found that stem cell deficiency may lead to a major cause of hair loss. This discovery will help scientists find a new method of treating hair loss.
Researchers at the University of Pennsylvania in the new issue of the U.S. “Journal of clinical examination,” the report said defects in hair follicle stem cells to hair growth makes it impossible to produce the source of cells, leading to hair loss. For men, a phenomenon known as male baldness, the symptoms started out as a head of hair, the hairline back, eventually leading to alopecia totalis; for women, the symptoms of hair is getting thin, but rarely cause alopecia to talis.
The researchers analyzed 54 men aged 40 to 65 years in the hair and scalp tissue was found, whether or not hair loss, hair loss, scalp tissue, the number of hair follicle stem cells are the same, the difference is, hair loss and scalp tissue The hair follicle stem cells did not produce the source of cells for hair growth, suggesting that the defect of hair follicle stem cells, so that the scalp can not grow hair.
Fix Qiaozhi Ke led the study, said Liss, previous studies that lead to hair loss because hair follicle stem cells no longer exists, but the latest study found that hair follicle stem cells are still only appeared flawed.
—–
J Clin Invest. doi:10.1172/JCI44478.
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.