日本研究人員在新一期美國《細胞—干細胞》雜志上報告說，動物實驗證實毛根缺乏一種膠原蛋白可同時導致脫發和白發。這一研究成果將有助于開發出治療脫發和白發的新藥。
東京醫科齒科大學教授西村榮美等研究人員報告說，他們發現ⅩⅦ型膠原蛋白的作用可使毛囊干細胞不會枯竭，從而防止脫發。同時，這種膠原蛋白在毛囊干細胞產生轉化生長因子－β的過程中也是不可缺少的。而轉化生長因子－β對色素干細胞的生成起著重要作用。
研究人員利用小鼠進行的實驗證實了他們的判斷。在正常情況下，毛色非白色的小鼠出生后約兩年就會因衰老而出現脫毛和毛變白的現象。研究人員通過基因技術使一些小鼠體內不能產生ⅩⅦ型膠原蛋白，結果它們在半年內就明顯地出現了白毛，大約10個月后，全身的毛就脫得差不多了。
在進一步的實驗中，研究人員把能生成ⅩⅦ型膠原蛋白的基因植入自身不能產生這種膠原蛋白的小鼠體內，結果小鼠能夠重新產生毛囊干細胞和色素干細胞，最終長出了一簇簇黑毛。
Hair Follicle Stem Cells Provide a Functional Niche for Melanocyte Stem Cells
Shintaro Tanimura, Yuko Tadokoro, Ken Inomata, Nguyen Thanh Binh, Wataru Nishie, Satoshi Yamazaki, Hiromitsu Nakauchi, Yoshio Tanaka, James R. McMillan, Daisuke Sawamura, Kim Yancey, Hiroshi Shimizu, Emi K. Nishimura
In most stem cell systems, the organization of the stem cell niche and the anchoring matrix required for stem cell maintenance are largely unknown. We report here that collagen XVII (COL17A1/BP180/BPAG2), a hemidesmosomal transmembrane collagen, is highly expressed in hair follicle stem cells (HFSCs) and is required for the maintenance not only of HFSCs but also of melanocyte stem cells (MSCs), which do not express Col17a1 but directly adhere to HFSCs. Mice lacking Col17a1 show premature hair graying and hair loss. Analysis of Col17a1-null mice revealed that COL17A1 is critical for the self-renewal of HFSCs through maintaining their quiescence and immaturity, potentially explaining the mechanism underlying hair loss in human COL17A1 deficiency. Moreover, forced expression of COL17A1 in basal keratinocytes, including HFSCs, in Col17a1-null mice rescues MSCs from premature differentiation and restores TGF-β signaling, demonstrating that HFSCs function as a critical regulatory component of the MSC niche.
