美國最新研究發(fā)現(xiàn),，干細胞缺陷可能是導致脫發(fā)的一個主要原因。這一發(fā)現(xiàn)將有助于科學家找到治療脫發(fā)的新方法,。
美國賓夕法尼亞大學的研究人員在新一期美國《臨床檢查雜志》上報告說,，毛囊干細胞缺陷使其無法產(chǎn)生讓頭發(fā)生長的源細胞，從而導致脫發(fā),。對男性來說,，這種現(xiàn)象稱為男性禿頂，其癥狀為頭部開始掉發(fā),，發(fā)際線后退,，最終導致全禿；對女性來說,，其癥狀為頭發(fā)越來越稀,，但很少導致全禿。
研究人員分析了54名40歲至65歲男子的頭發(fā)和頭皮組織,，結果發(fā)現(xiàn)，無論是脫發(fā)還是沒有脫發(fā)的頭皮組織中,，毛囊干細胞的數(shù)量都是相同的,，所不同的是，脫發(fā)頭皮組織中的毛囊干細胞沒有產(chǎn)生讓頭發(fā)生長的源細胞,，這表明毛囊干細胞產(chǎn)生了缺陷,，使頭皮無法長出頭發(fā)。
領導這一研究的喬治·科斯薩利斯說,，此前研究以為導致脫發(fā)的原因是毛囊干細胞已經(jīng)不存在了,，但最新的研究發(fā)現(xiàn)，毛囊干細胞還在，只是出現(xiàn)了缺陷,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
