日本东京医科齿科大学与金泽大学的一个研究小组近日发布消息，他们证实由于保持黑发的色素干细胞的基因损伤不断加重，人才会随着年龄的增长头发不断变白。该项研究有助于推动抗老化以及再生医疗药物的研究。美国《细胞》杂志发表了这一消息。
据介绍，色素干细胞存在于毛根与皮肤之间，正是由于其制造的色素细胞，人的头发才会保持黑色。如果这种干细胞减少或枯竭，人的头发就会变成白色，而其为何枯竭却一直不为人知。人们已知生物随着年龄的增长，基因的损伤就会不断加重，那么色素干细胞是不是也因为损伤加重而枯竭呢？为了证实这个设想，日本的研究人员用可造成基因损伤的放射线照射试验大鼠，使其出现与老化相似的状态，然后再检查大鼠的色素干细胞情况。结果发现大鼠的色素干细胞已经失去了分化再生的能力，由于缺少其制造的色素细胞，大鼠的毛色也变为了白色，从而证实了毛发变白的机理。
研究人员称，这项研究成果除了有助于人们揭开其他方面的老化之谜，还有助于推动抗白发药剂以及抗老化和再生医疗方面药物的研制。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
