Osteoarthritis (OA) is a general joint disease. Cartilage damage is associated with a decrease in the density of chondrocytes. Mesenchymal stem cells (MSCs) differentiate into adipocytes, osteocytes and chondrocytes, and are an excellent source of cell therapy. Cartilage-derived extracellular matrix (ECM) promotes chondrogenesis of MSCs. However, the role of MSCs stimulated by ECM is not well known in OA. The purpose of this study is to determine the role of specific factors generated by the application of ECM and umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs) in managing OA symptoms. Cartilage acellular matrix (CAM), which is a cartilage-derived ECM, was used to promote the chondrogenesis of UCB-MSCs. Induced MSCs were analyzed using chondrogenic markers (aggrecan, collagen type 2, and SOX9) and bone morphogenic protein 6 (BMP6). BMP6 is known to be involved in early chondrogenesis of MSCs. As a result, treatment with CAM significantly increased the expression of chondrogenic markers and BMP6 in UCB-MSCs. Treatment with recombinant human BMP6 also dramatically increased the levels of chondrogenic markers in UCB-MSCs. In addition, UCB-MSCs and CAM were used to evaluate OA symptom improvement in a rabbit articular cruciate ligament transection (ACLT) model. Application of UCB-MSCs and CAM enhanced not only the structure and synthesis of proteoglycan and collagen type 2 but also anti-inflammatory effects in both rabbit joint and synovial fluid. Moreover, the detection of human cells and involvement of BMP6 were confirmed in rabbit cartilage tissues. This study indicates that therapeutic potential of UCB-MSCs with CAM is mediated via BMP6 in OA.

中文翻译：

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人脐带血间充质干细胞结合通过骨形态发生蛋白6介导的软骨无细胞基质在兔关节十字韧带横断模型中的治疗作用。

骨关节炎（OA）是一种普通的关节疾病。软骨损伤与软骨细胞密度的降低有关。间充质干细胞（MSC）分化为脂肪细胞，骨细胞和软骨细胞，是细胞疗法的极好来源。软骨衍生的细胞外基质（ECM）促进MSC的软骨形成。但是，在OA中，由ECM刺激的MSC的作用尚不清楚。这项研究的目的是确定由应用ECM和脐血来源的间充质干细胞（UCB-MSC）产生的特定因素在治疗OA症状中的作用。软骨脱细胞基质（CAM）是一种软骨衍生的ECM，用于促进UCB-MSC的软骨形成。使用软骨生成标记（aggrecan，2型胶原和SOX9）和骨形态发生蛋白6（BMP6）分析诱导的MSC。已知BMP6参与MSC的早期软骨形成。结果，用CAM处理可显着增加UCB-MSC中软骨生成标记和BMP6的表达。重组人BMP6的治疗还大大增加了UCB-MSC中的软骨生成标记物水平。此外，UCB-MSC和CAM用于评估兔关节十字韧带横切（ACLT）模型中OA症状的改善。UCB-MSC和CAM的应用不仅增强了蛋白聚糖和2型胶原蛋白的结构和合成，而且还增强了兔关节和滑液的抗炎作用。此外，在兔软骨组织中证实了人细胞的检测和BMP6的参与。这项研究表明，具有CAM的UCB-MSC的治疗潜力是通过OA中的BMP6介导的。