Ding Xiaoquan, Zhang Yujun, Huang Yuelong, Liu Songyang, Lu Houshan, Sun Tiezheng
Arthritis Clinic and Research Center, People's Hospital, Peking University, Beijing China.
Clinical Institute of Molecular Biology, People's Hospital, Peking University, Beijing China.
Int Immunopharmacol. 2015 May;26(1):153-61. doi: 10.1016/j.intimp.2015.03.024. Epub 2015 Mar 28.
To detect the expression of cadherin-11 and its correlation with synovitis in osteoarthritis (OA), to explore the mechanism of over expression of cadherin-11 and its role in migratory or invasive capacity of fibroblast-like synoviocytes (FLS).
Synovitis severity was recorded according to Krenn's scoring system in 25 osteoarthritis patients undergoing total knee arthroplasty. Cadherin-11 expression in OA synoviums and its correlation with synovitis score and systemic inflammation markers were explored. After induction with Interleukin-1 beta (IL-1β) or tumor necrosis factor-alpha (TNF-α),cadherin-11 expression on OA FLS was assessed by qPCR and western blot,the capacity of migration and invasion of OA FLS was tested by transwell assay, and matrix metalloproteinase-2 production was assessed with ELISA as cadherin-11 expression was up regulated after infection with cadherin-11 cDNA-containing lentivirus, also when cadherin-11 expression was knocked down after infection with cadherin 11 shRNA containing lentivirus.
Cadherin-11 expression in OA synovium showed significant differences among different grades of synovitis. Cadherin-11 in the lining layer was positively correlated with hyperplasia of the lining layer, density of the resident cells, inflammatory infiltrate, total synovitis score and D-dimer. Cadherin-11 in the sublining layer was positively correlated with the density of the resident cells, inflammatory infiltrate, total synovitis score and erythrocyte sedimentation rate. IL-1β or TNF-α could up-regulate cadherin-11 expression on OA FLS at transcriptional and protein level. Over expression of cadherin-11 increased migratory or invasive capacity of OA FLS, while cadherin-11 knock down reduced migratory or invasive capacity and MMP-2 production in OA FLS.
The over expression of cadherin-11 in osteoarthritis is positively correlated with synovitis severity, and can be driven by proinflammatory cytokines on OA FLS; cadherin-11 increases migratory or invasive capacity and MMP-2 production of fibroblast-like synoviocytes of osteoarthritis.
检测钙黏蛋白-11在骨关节炎（OA）中的表达及其与滑膜炎的相关性，探讨钙黏蛋白-11过表达的机制及其在成纤维样滑膜细胞（FLS）迁移或侵袭能力中的作用。
根据Krenn评分系统记录25例行全膝关节置换术的骨关节炎患者的滑膜炎严重程度。探讨钙黏蛋白-11在OA滑膜中的表达及其与滑膜炎评分和全身炎症标志物的相关性。用白细胞介素-1β（IL-1β）或肿瘤坏死因子-α（TNF-α）诱导后，通过qPCR和western blot评估OA FLS上钙黏蛋白-11的表达，通过transwell试验检测OA FLS的迁移和侵袭能力，并用ELISA评估基质金属蛋白酶-2的产生，因为在用含钙黏蛋白-11 cDNA的慢病毒感染后钙黏蛋白-11表达上调，在用含钙黏蛋白11 shRNA的慢病毒感染后钙黏蛋白-11表达被敲低时也是如此。
钙黏蛋白-11在OA滑膜中的表达在不同等级的滑膜炎之间存在显著差异。衬里层中的钙黏蛋白-11与衬里层增生、驻留细胞密度、炎症浸润、总滑膜炎评分和D-二聚体呈正相关。滑膜下层中的钙黏蛋白-11与驻留细胞密度、炎症浸润、总滑膜炎评分和红细胞沉降率呈正相关。IL-1β或TNF-α可在转录和蛋白水平上调OA FLS上钙黏蛋白-11的表达。钙黏蛋白-11的过表达增加了OA FLS的迁移或侵袭能力，而钙黏蛋白-11的敲低降低了OA FLS的迁移或侵袭能力以及MMP-2的产生。
骨关节炎中钙黏蛋白-11的过表达与滑膜炎严重程度呈正相关，并且可由OA FLS上的促炎细胞因子驱动；钙黏蛋白-11增加了骨关节炎成纤维样滑膜细胞的迁移或侵袭能力以及MMP-2的产生。
