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In vivo effect of opticin deficiency in cartilage in a surgically induced mouse model of osteoarthritis

机译:手术诱发的骨关节炎小鼠模型中视黄蛋白缺乏症在软骨中的体内作用

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The SLRP opticin (OPTC) has been demonstrated to be produced and degraded in osteoarthritic (OA) human cartilage. Here, we investigated the in vivo effect of OPTC deficiency in OA cartilage. OA was induced in 10-week-old Optc ?/? and Optc +/+ mice. Ten weeks post-surgery, cartilage was processed for histology and immunohistochemistry. SLRP expression was determined in non-operated mouse cartilage. OA Optc ?/? demonstrated significant protection against cartilage degradation. Data revealed that in non-operated Optc ?/? cartilage, expression of SLRPs lumican and epiphycan was up-regulated at day 3 and in 10-week-olds (p?≤?0.039), and fibromodulin down-regulated in 10-week-olds (p?=?0.001). Immunohistochemistry of OA mice showed a similar pattern. In OA Optc ?/? cartilage, markers of degradation and complement factors were all down-regulated (p?≤?0.038). In OA Optc ?/? cartilage, collagen fibers were thinner and better organized (p?=?0.038) than in OA Optc +/+ cartilage. The protective effect of OPTC deficiency during OA results from an overexpression of lumican and epiphycan, known to bind and protect collagen fibers, and a decrease in fibromodulin, contributing to a reduction in the complement activation/inflammatory process. This work suggests that the evaluation of the composition of the different SLRPs in OA cartilage could be applied as a new tool for OA prognosis classification.
机译:已经证明SLRP视蛋白(OPTC)在骨关节炎(OA)人软骨中产生并降解。在这里,我们调查了OPTC缺乏对OA软骨的体内作用。在10周大的Optc?/?中诱发了OA。和Optc + / +鼠标。手术后十周,对软骨进行组织学和免疫组织化学处理。在非手术小鼠软骨中确定SLRP表达。 OA Optc?/?表现出显着的抗软骨降解保护作用。数据显示,在非运营中的Optc?/?软骨,在第3天和10周龄时,SLUMs lumican和epiphycan的表达上调(p≤≤0.039),而在10周龄时纤维调节蛋白下调(p≤0.001)。 OA小鼠的免疫组织化学显示相似的模式。在OA Optc中?软骨,降解标志物和补体因子均被下调(p≤≤0.038)。在OA Optc中?软骨中,胶原纤维比OA Optc + / +软骨中的纤维更细,组织更好(p?=?0.038)。 OA期间OPTC缺乏的保护作用是由于已知可以结合和保护胶原纤维的Lumican和Epiphycan的过表达以及纤维调节蛋白的减少,从而导致补体激活/炎症过程的减少而导致的。这项工作表明,OA软骨中不同SLRPs组成的评估可以用作OA预后分类的新工具。

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