Helminen H J, Säämänen A-M, Salminen H, Hyttinen M M
Department of Anatomy, University of Kuopio, Finland.
Rheumatology (Oxford). 2002 Aug;41(8):848-56. doi: 10.1093/rheumatology/41.8.848.
The development of transgenic technology has made possible the generation of targeted gene-mutated mouse lines suitable for use in experimental osteoarthritis (OA) research. Transgenic mice harbouring mutations in cartilage collagen types II and IX develop early-onset OA and are therefore promising models of age-related OA, even though the mice often show signs of chondrodysplasia. Also, mouse lines harbouring other engineered mutations of the extracellular molecules have given rise to early OA. The molecular background of a few spontaneous mutations in mice has also been clarified and the characterization of the OA phenotype is now in progress. These mutations cause severe chondrodysplasia and death in homozygous mice, but the heterozygous offspring develop the early-onset OA phenotype.
转基因技术的发展使得生成适用于实验性骨关节炎(OA)研究的靶向基因突变小鼠品系成为可能。携带II型和IX型软骨胶原蛋白突变的转基因小鼠会发生早发性OA,因此是与年龄相关OA的有前景的模型,尽管这些小鼠常常表现出软骨发育异常的迹象。此外,携带细胞外分子其他工程突变的小鼠品系也引发了早发性OA。小鼠中一些自发突变的分子背景也已得到阐明,目前正在对OA表型进行特征描述。这些突变在纯合小鼠中会导致严重的软骨发育异常和死亡,但杂合子后代会出现早发性OA表型。