Liu Qin, Lu Zhenhui, Wu Huayu, Zheng Li
Medical and Scientific Research Center, Guangxi Medical University; Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi, P.R. China.
Tohoku J Exp Med. 2015 Mar;235(3):201-13. doi: 10.1620/tjem.235.201.
Articular cartilage is characterized by the lack of blood vessels and has a poor self-healing potential. Limited cell numbers and dedifferentiation of chondrocytes when expanded in vitro are the major obstacles of autologous chondrocyte implantation. Autologous chondrocyte implantation is a cell-based treatment that can be used as a second-line measure to regenerate chondral or osteochondral defects in younger, active patients. There is an urgent need to find an effective chondrogenic protection agent alleviating or inhibiting chondrocyte dedifferentiation. In this study, we explored the effect of taurine (2-aminoethane sulfonic acid) on proliferation and phenotype maintenance of human articular chondrocytes by analyzing the cell proliferation, morphology, viability, and expression of cartilage specific mRNAs and proteins. Primary chondrocytes were isolated from human articular cartilage tissues. Results showed that taurine effectively promoted chondrocyte growth and enhanced accumulation of glycosaminoglycans and collagens in the conditioned media of chondrocytes. Moreover, taurine exposure caused significant increases in the relative expression levels of mRNAs for cartilage specific markers, including aggrecan, collagen type II and SOX9. Aggrecan is a cartilage-specific proteoglycan, and SOX9 is a chondrogenic transcription factor. In contrast, the mRNA expression of collagen type I, a marker for chondrocyte dedifferentiation, was significantly decreased in cells treated with taurine, indicating that taurine inhibits the chondrocyte dedifferentiation. This study reveals that taurine is effective in proliferation promotion and phenotype maintenance of chondrocytes. Thus, taurine may be a useful pro-chondrogenic agent for autologous chondrocyte implantation in the treatment of cartilage repair.
关节软骨的特点是缺乏血管,自我修复能力差。体外培养时软骨细胞数量有限以及去分化是自体软骨细胞移植的主要障碍。自体软骨细胞移植是一种基于细胞的治疗方法,可作为年轻、活跃患者软骨或骨软骨缺损再生的二线治疗措施。迫切需要找到一种有效的软骨生成保护剂来减轻或抑制软骨细胞去分化。在本研究中,我们通过分析细胞增殖、形态、活力以及软骨特异性mRNA和蛋白质的表达,探讨了牛磺酸(2-氨基乙磺酸)对人关节软骨细胞增殖和表型维持的影响。原代软骨细胞从人关节软骨组织中分离出来。结果表明,牛磺酸有效地促进了软骨细胞生长,并增强了软骨细胞条件培养基中糖胺聚糖和胶原蛋白的积累。此外,牛磺酸处理导致软骨特异性标志物(包括聚集蛋白聚糖、II型胶原蛋白和SOX9)的mRNA相对表达水平显著增加。聚集蛋白聚糖是一种软骨特异性蛋白聚糖,而SOX9是一种软骨生成转录因子。相反,在牛磺酸处理的细胞中,作为软骨细胞去分化标志物的I型胶原蛋白的mRNA表达显著降低,表明牛磺酸抑制了软骨细胞去分化。本研究表明,牛磺酸在促进软骨细胞增殖和维持表型方面有效。因此,牛磺酸可能是自体软骨细胞移植治疗软骨修复中一种有用的促软骨生成剂。