Zhao Qiaofeng, Koyama Satoshi, Yoshihara Nagisa, Takagi Atsushi, Komiyama Etsuko, Wada Akino, Oka Akira, Ikeda Shigaku
Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
The Institute of Medical Sciences, Tokai University, Kanagawa 259-1193, Japan.
Biomedicines. 2021 Jul 19;9(7):840. doi: 10.3390/biomedicines9070840.
We recently discovered a nonsynonymous variant in the coiled-coil alpha-helical rod protein 1 () gene within the alopecia areata (AA) risk haplotype. We also reported that the engineered mice with this risk allele exhibited. To investigate more about the involvement of the gene in AA pathogenesis, we developed an AA model using C57BL/6N gene knockout mice. In this study, mice (6-8 weeks) were divided into two groups: mice and wild-type (WT) littermates. Both groups were subjected to a water avoidance stress (WAS) test. Eight weeks after the WAS test, 25% of mice exhibited non-inflammatory foci of alopecia on the dorsal skin. On the other hand, none of wild-type littermates cause hair loss. The foci resembled human AA in terms of gross morphology, trichoscopic findings and histological findings. Additionally, gene expression microarray analysis of mice revealed abnormalities of hair related genes compared to the control. Our results strongly suggest that is associated with AA pathogenesis and that mice are a good model for investigating AA.
我们最近在斑秃（AA）风险单倍型内的卷曲螺旋α-螺旋杆蛋白1（）基因中发现了一个非同义变体。我们还报道了携带这种风险等位基因的工程小鼠表现出。为了进一步研究该基因在AA发病机制中的作用，我们利用C57BL/6N基因敲除小鼠建立了一个AA模型。在本研究中，将6-8周龄的小鼠分为两组：基因敲除小鼠和野生型（WT）同窝小鼠。两组均接受避水应激（WAS）试验。WAS试验8周后，25%的基因敲除小鼠背部皮肤出现非炎性脱发灶。另一方面，野生型同窝小鼠均未出现脱发。这些病灶在大体形态、毛发镜检查结果和组织学检查结果方面与人类AA相似。此外，与对照组相比，基因敲除小鼠的基因表达微阵列分析显示毛发相关基因存在异常。我们的结果强烈表明该基因与AA发病机制有关，并且基因敲除小鼠是研究AA的良好模型。
