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靶向破坏导致不同器官受累的巨血小板减少症的人类MYH9小鼠直系同源基因:杂合敲除小鼠的血液学、肾脏病学和耳科学研究

Targeted disruption of mouse ortholog of the human MYH9 responsible for macrothrombocytopenia with different organ involvement: hematological, nephrological, and otological studies of heterozygous KO mice.

作者信息

Matsushita Tadashi, Hayashi Hideo, Kunishima Shinji, Hayashi Mutsuharu, Ikejiri Makoto, Takeshita Kyosuke, Yuzawa Yukio, Adachi Tatsuya, Hirashima Kanji, Sone Michihiko, Yamamoto Koji, Takagi Akira, Katsumi Akira, Kawai Kumi, Nezu Tomoyo, Takahashi Masahide, Nakashima Tsutomu, Naoe Tomoki, Kojima Tetsuhito, Saito Hidehiko

机构信息

Department of Hematology, Nagoya University Graduate School of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 2004 Dec 24;325(4):1163-71. doi: 10.1016/j.bbrc.2004.10.147.

Abstract

Among three different isoforms of non-muscle myosin heavy chains (NMMHCs), only NMMHCA is associated with inherited human disease, called MYH9 disorders, characterized by macrothrombocytopenia and characteristic granulocyte inclusions. Here targeted gene disruption was performed to understand fundamental as well as pathological role of the gene for NMMHCA, MYH9. Heterozygous intercrosses yielded no homozygous animals among 552 births, suggesting that MYH9 expression is required for embryonic development. In contrast, MYH9+/- mice were viable and fertile without gross anatomical, hematological, and nephrological abnormalities. Immunofluorescence analysis also showed the normal cytoplasmic distribution of NMMHCA. We further measured the auditory brainstem response and found two of six MYH9+/- mice had hearing losses, whereas the remaining four were comparable to wild-type mice. Such observation may parallel the diverse expression of Alport's manifestations of human individuals with MYH9 disorders and suggest the limited requirement of the gene for maintenance and function of specific organs.

摘要

在非肌肉肌球蛋白重链(NMMHCs)的三种不同同工型中,只有NMMHCA与遗传性人类疾病相关,称为MYH9障碍,其特征为大血小板减少症和特征性粒细胞包涵体。在此进行了靶向基因破坏,以了解NMMHCA基因(MYH9)的基本以及病理作用。杂合子杂交在552次出生中未产生纯合动物,这表明MYH9表达对于胚胎发育是必需的。相比之下,MYH9+/-小鼠存活且可育,没有明显的解剖学、血液学和肾脏病学异常。免疫荧光分析还显示NMMHCA在细胞质中的分布正常。我们进一步测量了听觉脑干反应,发现六只MYH9+/-小鼠中有两只存在听力损失,而其余四只与野生型小鼠相当。这种观察结果可能与患有MYH9障碍的人类个体中阿尔波特综合征表现的多样表达相似,并表明该基因对特定器官的维持和功能的需求有限。

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