日本東京醫(yī)科齒科大學(xué)與金澤大學(xué)的一個研究小組近日發(fā)布消息,，他們證實由于保持黑發(fā)的色素干細(xì)胞的基因損傷不斷加重，人才會隨著年齡的增長頭發(fā)不斷變白,。該項研究有助于推動抗老化以及再生醫(yī)療藥物的研究,。美國《細(xì)胞》雜志發(fā)表了這一消息。
據(jù)介紹,，色素干細(xì)胞存在于毛根與皮膚之間,，正是由于其制造的色素細(xì)胞，人的頭發(fā)才會保持黑色,。如果這種干細(xì)胞減少或枯竭,，人的頭發(fā)就會變成白色，而其為何枯竭卻一直不為人知,。人們已知生物隨著年齡的增長,，基因的損傷就會不斷加重，那么色素干細(xì)胞是不是也因為損傷加重而枯竭呢,？為了證實這個設(shè)想,，日本的研究人員用可造成基因損傷的放射線照射試驗大鼠，使其出現(xiàn)與老化相似的狀態(tài),，然后再檢查大鼠的色素干細(xì)胞情況,。結(jié)果發(fā)現(xiàn)大鼠的色素干細(xì)胞已經(jīng)失去了分化再生的能力，由于缺少其制造的色素細(xì)胞,，大鼠的毛色也變?yōu)榱税咨?，從而證實了毛發(fā)變白的機(jī)理,。
研究人員稱，這項研究成果除了有助于人們揭開其他方面的老化之謎,，還有助于推動抗白發(fā)藥劑以及抗老化和再生醫(yī)療方面藥物的研制,。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell, Volume 137, 12 June 2009 doi:10.1016/j.cell.2009.03.037
Genotoxic Stress Abrogates Renewal of Melanocyte Stem Cells by Triggering Their Differentiation
Ken Inomata1,2,3,Takahiro Aoto1,4,Nguyen Thanh Binh1,Natsuko Okamoto1,5,Shintaro Tanimura1,3,Tomohiko Wakayama6,Shoichi Iseki6,Eiji Hara7,Takuji Masunaga2,Hiroshi Shimizu3andEmi K. Nishimura1,4,,
1 Division of Stem Cell Medicine, Center for Cancer and Stem Cell Research, Cancer Research Institute, Kanazawa University, 13-1 Takaramachi, Kanazawa, Ishikawa 920-0934, Japan
2 Fundamental Research Laboratories, KOSé Corporation, 1-18-4 Azusawa, Itabashi-ku, Tokyo 174-0051, Japan
3 Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita-ku, Sapporo 060-8638, Japan
4 Department of Stem Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan
5 Department of Dermatology, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawaharacho, Sakyo-Ku, Kyoto, 606-8507, Japan
6 Department of Histology and Embryology, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-0934, Japan
7 Division of Cancer Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 3-10-6, Ariake, Koto-ku, Tokyo 135-8550, Japan
Somatic stem cell depletion due to the accumulation of DNA damage has been implicated in the appearance of aging-related phenotypes. Hair graying, a typical sign of aging in mammals, is caused by the incomplete maintenance of melanocyte stem cells (MSCs) with age. Here, we report that irreparable DNA damage, as caused by ionizing radiation, abrogates renewal of MSCs in mice. Surprisingly, the DNA-damage response triggers MSC differentiation into mature melanocytes in the niche, rather than inducing their apoptosis or senescence. The resulting MSC depletion leads to irreversible hair graying. Furthermore, deficiency of Ataxia-telangiectasia mutated (ATM), a central transducer kinase of the DNA-damage response, sensitizes MSCs to ectopic differentiation, demonstrating that the kinase protects MSCs from their premature differentiation by functioning as a stemness checkpoint to maintain the stem cell quality and quantity.
