美国最新研究发现,干细胞缺陷可能是导致脱发的一个主要原因。这一发现将有助于科学家找到治疗脱发的新方法。
美国宾夕法尼亚大学的研究人员在新一期美国《临床检查杂志》上报告说,毛囊干细胞缺陷使其无法产生让头发生长的源细胞,从而导致脱发。对男性来说,这种现象称为男性秃顶,其症状为头部开始掉发,发际线后退,最终导致全秃;对女性来说,其症状为头发越来越稀,但很少导致全秃。
研究人员分析了54名40岁至65岁男子的头发和头皮组织,结果发现,无论是脱发还是没有脱发的头皮组织中,毛囊干细胞的数量都是相同的,所不同的是,脱发头皮组织中的毛囊干细胞没有产生让头发生长的源细胞,这表明毛囊干细胞产生了缺陷,使头皮无法长出头发。
领导这一研究的乔治·科斯萨利斯说,此前研究以为导致脱发的原因是毛囊干细胞已经不存在了,但最新的研究发现,毛囊干细胞还在,只是出现了缺陷。(生物谷Bioon.com)
生物谷推荐原文出处:
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.