Institute of Biology and Chemistry of Proteins, LBTi, CNRS-LIMR 5305, Lyon, France.
Tissue Eng Part C Methods. 2013 Aug;19(8):652-64. doi: 10.1089/ten.TEC.2012.0396. Epub 2013 Apr 15.
Because articular cartilage does not self-repair, tissue-engineering strategies should be considered to regenerate this tissue. Autologous chondrocyte implantation is already used for treatment of focal damage of articular cartilage. Unfortunately, this technique includes a step of cell amplification, which results in dedifferentiation of chondrocytes, with expression of type I collagen, a protein characteristic of fibrotic tissues. Therefore, the risk of producing a fibrocartilage exists. The aim of this study was to propose a new strategy for authorizing the recovery of the differentiated status of the chondrocytes after their amplification on plastic. Because the bone morphogenetic protein (BMP)-2 and the transforming growth factor (TGF)-β1 are cytokines both proposed as stimulants for cartilage repair, we undertook a detailed comparative analysis of their biological effects on chondrocytes. As a cellular model, we used mouse chondrocytes after their expansion on plastic and we tested the capability of BMP-2 or TGF-β1 to drive their redifferentiation, with special attention given to the nature of the proteins synthesized by the cells. To prevent any fibrotic character of the newly synthesized extracellular matrix, we silenced type I collagen by transfecting small interfering RNA (siRNA) into the chondrocytes, before their exposure to BMP-2 or TGF-β1. Our results showed that addition of siRNA targeting the mRNA encoded by the Col1a1 gene (Col1a1 siRNA) and BMP-2 represents the most efficient combination to control the production of cartilage-characteristic collagen proteins. To go one step further toward scaffold-based cartilage engineering, Col1a1 siRNA-transfected chondrocytes were encapsulated in agarose hydrogel and cultured in vitro for 1 week. The analysis of the chondrocyte-agarose constructs by using real-time polymerase chain reaction, Western-blotting, immunohistochemistry, and electron microscopy techniques demonstrated that the BMP-2/Col1a1 siRNA combination is effective in reinitializing correct production and assembly of the cartilage-characteristic matrix in agarose hydrogel, without production of type I collagen. Because agarose is known to favor long-term expression of the chondrocyte phenotype and agarose-based hydrogels are approved for clinical trials, this strategy appears very promising to repair hyaline cartilage.
由于关节软骨不能自我修复,因此应考虑采用组织工程策略来再生这种组织。自体软骨细胞植入术已经用于治疗关节软骨的局灶性损伤。不幸的是,该技术包括细胞扩增步骤,这会导致软骨细胞去分化,表达Ⅰ型胶原,这是一种纤维组织特征性蛋白。因此,存在产生纤维软骨的风险。本研究旨在提出一种新策略,以允许在塑料上扩增后的软骨细胞恢复其分化状态。由于骨形态发生蛋白(BMP)-2 和转化生长因子(TGF)-β1 均被提议作为软骨修复的刺激物,因此我们对它们对软骨细胞的生物学效应进行了详细的比较分析。作为细胞模型,我们使用在塑料上扩增后的小鼠软骨细胞,并测试了 BMP-2 或 TGF-β1 驱动其再分化的能力,特别关注细胞合成的蛋白质的性质。为了防止新合成的细胞外基质具有纤维特征,我们在将软骨细胞暴露于 BMP-2 或 TGF-β1 之前,通过转染小干扰 RNA(siRNA)沉默 Col1a1 基因编码的 mRNA。我们的结果表明,添加靶向 Col1a1 基因编码的 mRNA 的 siRNA(Col1a1 siRNA)和 BMP-2 的组合是控制软骨特征性胶原蛋白产生的最有效组合。为了进一步进行基于支架的软骨工程,将 Col1a1 siRNA 转染的软骨细胞包封在琼脂糖水凝胶中,并在体外培养 1 周。通过实时聚合酶链反应、Western 印迹、免疫组织化学和电子显微镜技术对软骨细胞-琼脂糖构建体进行分析,证明 BMP-2/Col1a1 siRNA 组合可有效重新启动正确的软骨特征性基质的产生和组装,而不产生Ⅰ型胶原。由于已知琼脂糖有利于长期表达软骨细胞表型,并且琼脂糖基水凝胶已被批准用于临床试验,因此该策略在修复透明软骨方面具有很大的应用前景。