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首页> 外文期刊>Osteoarthritis and cartilage >Osteoarthritis-like changes in the heterozygous sedc mouse associated with the HtrA1-Ddr2-Mmp-13 degradative pathway: A new model of osteoarthritis
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Osteoarthritis-like changes in the heterozygous sedc mouse associated with the HtrA1-Ddr2-Mmp-13 degradative pathway: A new model of osteoarthritis

机译：与HtrA1-Ddr2-Mmp-13降解途径相关的杂合子sedc小鼠中的骨关节炎样变化：骨关节炎的新模型

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Objective: To test the hypothesis that the spondyloepiphyseal dysplasia congenita (. sedc) heterozygous (. sedc/+) mouse, a . COL2A1 mutant, is a model for the study of osteoarthritis (OA) in the absence of dwarfism and to investigate the presence of HtrA1, Ddr2, and Mmp-13 and their possible involvement in a universal mechanism leading to OA. Design: Whole mount skeletons of adult animals were analyzed to determine whether . sedc/+ mice exhibit dwarfism. To characterize progression of osteoarthritic degeneration over time, knee and temporomandibular joints from . sedc/+ and wild-type mice were analyzed histologically, and severity of articular cartilage degradation was graded using the Osteoarthritis Research Society International (OARSI) scoring system. Immunohistochemistry was used to detect changes in expression of HtrA1, Ddr2, and Mmp-13 in articular cartilage of knees. Results: As previously reported, the . sedc/+ skeleton morphology was indistinguishable from wild type, and skeletal measurements revealed no significant differences. The . sedc/+ mouse did, however, show significantly higher OARSI scores in knee (9, 12 and 18 months) and temporomandibular joints at all ages examined. Histological staining showed regions of proteoglycan degradation as early as 2 months in both temporomandibular and knee joints of the mutant. Cartilage fissuring and erosion were observed to begin between 2 and 6 months in temporomandibular joints and 9 months in knee joints from . sedc/+ mice. Immunohistochemistry of mutant knee articular cartilage showed increased expression of HtrA1, Ddr2, and Mmp-13 compared to wild type, which upregulation preceded fibrillation and fissuring of the articular surfaces. Conclusions: With regard to skeletal morphology, the . sedc/+ mouse appears phenotypically normal but develops premature OA as hypothesized. We conclude that the . sedc/+ mouse is a useful model for the study of OA in individuals with overtly normal skeletal structure and a predisposition for articular cartilage degeneration.
机译：目的：检验假说先天性脊柱干phy发育不良（。sedc）杂合子（。sedc / +）小鼠。 COL2A1突变体是在不存在侏儒症的情况下研究骨关节炎（OA）并研究HtrA1，Ddr2和Mmp-13的存在及其可能参与导致OA的普遍机制的模型。设计：分析成年动物的整个骨骼，以确定是否。 sedc / +小鼠表现出侏儒症。表征随着时间推移，膝关节和颞下颌关节的骨关节炎变性的进展。对sedc / +和野生型小鼠进行组织学分析，并使用国际骨关节炎研究协会（OARSI）评分系统对关节软骨退化的严重程度进行分级。免疫组织化学用于检测膝盖关节软骨中HtrA1，Ddr2和Mmp-13表达的变化。结果：如先前报道，。 sedc / +骨骼形态与野生型没有区别，骨骼测量显示无显着差异。的。 sedc / +小鼠在所有年龄段的膝盖（9、12和18个月）和颞下颌关节的OARSI评分均明显更高。组织学染色显示，在该突变体的颞下颌和膝关节中，蛋白聚糖降解的区域早于2个月。颞下颌关节软骨裂变和侵蚀发生在2至6个月之间，膝关节软骨裂变和侵蚀开始于9个月。 sedc / +小鼠。与野生型相比，突变型膝关节软骨的免疫组织化学显示HtrA1，Ddr2和Mmp-13的表达增加，后者在原纤维形成和关节表面裂开之前上调。结论：关于骨骼形态，。 sedc / +小鼠在表型上看似正常，但如假设的那样会发展为过早的OA。我们得出结论。 sedc / +小鼠是研究骨灰质正常且易患关节软骨退变的个体的OA的有用模型。

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