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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Targeted disruption of Mig-6 in the mouse genome leads to early onset degenerative joint disease
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Targeted disruption of Mig-6 in the mouse genome leads to early onset degenerative joint disease

机译：小鼠基因组中Mig-6的靶向破坏会导致早期变性性关节疾病

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摘要

Degenerative joint disease, also known as osteoarthritis, is the most common joint disorder in human beings. The molecular mechanism underlying this disease is not fully understood. Here, we report that disruption of mitogen-inducible gene 6 (Mig-6) in mice by homologous recombination leads to early onset degenerative joint disease, which is revealed by simultaneous enlargement and deformity of multiple joints, degradation of articular cartilage, and the development of bony outgrowths or osteophyte formation within joint space. The osteophyte formation appears to be derived from proliferation of mesenchymal progenitor cells followed by differentiation into chondrocytes. Absence of the Rag2 gene does not rescue the joint phenotype, excluding a role for the acquired immune system in the development of this disease. Our results provide insight into the mechanism of osteoarthritis by showing that loss of Mig-6 leads to early onset of this disease, implying that this gene or its pathway is important in normal joint maintenance. Because of the striking similarity of osteoarthritis in humans and mice, the Mig-6 mutant mouse should provide a useful animal model for studying the mechanism of this disease and for testing drugs or therapies for treating osteoarthritis.
机译：退化性关节疾病，也称为骨关节炎，是人类最常见的关节疾病。这种疾病的分子机制尚不完全清楚。在这里，我们报道通过同源重组破坏小鼠中的促分裂原诱导基因6（Mig-6）导致早期退化性关节疾病，这通过多个关节的同时扩大和畸变，关节软骨的退化以及发育得到揭示。关节腔内骨长出或骨赘形成。骨赘的形成似乎源自间充质祖细胞的增殖，然后分化为软骨细胞。 Rag2基因的缺乏不能挽救关节表型，除了获得性免疫系统在这种疾病发展中的作用外。我们的结果通过显示Mig-6的缺失导致该病的早期发作，从而提供了对骨关节炎机制的洞察力，这表明该基因或其途径在正常的关节维​​持中很重要。由于人类和小鼠的骨关节炎具有惊人的相似性，因此Mig-6突变小鼠应该为研究这种疾病的机理以及测试治疗骨关节炎的药物或疗法提供有用的动物模型。

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