Ma Liang, Liu Jian, Wu Tobey, Plikus Maksim, Jiang Ting-Xin, Bi Qun, Liu Yi-Hsin, Müller-Röver Sven, Peters Heiko, Sundberg John P, Maxson Rob, Maas Richard L, Chuong Cheng-Ming
Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Development. 2003 Jan;130(2):379-89. doi: 10.1242/dev.00201.
Msx2-deficient mice exhibit progressive hair loss, starting at P14 and followed by successive cycles of wavelike regrowth and loss. During the hair cycle, Msx2 deficiency shortens anagen phase, but prolongs catagen and telogen. Msx2-deficient hair shafts are structurally abnormal. Molecular analyses suggest a Bmp4/Bmp2/Msx2/Foxn1 acidic hair keratin pathway is involved. These structurally abnormal hairs are easily dislodged in catagen implying a precocious exogen. Deficiency in Msx2 helps to reveal the distinctive skin domains on the same mouse. Each domain cycles asynchronously - although hairs within each skin domain cycle in synchronized waves. Thus, the combinatorial defects in hair cycling and differentiation, together with concealed skin domains, account for the cyclic alopecia phenotype.
Msx2基因缺陷型小鼠从出生后第14天开始出现进行性脱发,随后是连续的波浪状再生和脱落循环。在毛发周期中,Msx2基因缺陷会缩短生长期,但延长退行期和休止期。Msx2基因缺陷型毛发的毛干结构异常。分子分析表明,存在一条Bmp4/Bmp2/Msx2/Foxn1酸性毛发角蛋白信号通路。这些结构异常的毛发在退行期很容易脱落,这意味着外根鞘早熟。Msx2基因缺陷有助于揭示同一只小鼠身上不同的皮肤区域。每个区域的毛发循环是异步的——尽管每个皮肤区域内的毛发以同步波浪的形式循环。因此,毛发循环和分化中的组合缺陷,以及隐藏的皮肤区域,共同导致了周期性脱发的表型。