Gelse Kolja, von der Mark Klaus, Aigner Thomas, Park Jung, Schneider Holm
University of Erlangen-Nuernberg, Erlangen, Germany.
Arthritis Rheum. 2003 Feb;48(2):430-41. doi: 10.1002/art.10759.
To investigate the repair of partial-thickness lesions in rat articular cartilage by combining cell transplantation with transfer of growth factor complementary DNA (cDNA).
Mesenchymal cells isolated from rib perichondrium were infected ex vivo with adenoviral vectors carrying bone morphogenetic protein 2 (BMP-2) or insulin-like growth factor 1 (IGF-1) cDNA. The cells were suspended in fibrin glue and applied to mechanically induced partial-thickness cartilage lesions in the patellar groove of the rat femur. The filling of the defects was quantified and the quality and integration of the newly formed tissue were assessed by histochemical and immunohistochemical methods. Uninfected cells or cells infected with a LacZ reporter gene vector served as controls.
Transplanted cells were able to attach to the wounded articular cartilage and were not displaced from the lesions by joint movement. Cells infected with both adenoviral vectors AdBMP-2 and AdIGF-1 produced repair cartilage of hyaline morphology containing a type II collagen-positive but type I collagen-negative proteoglycan-rich matrix that restored the articular surface in most lesions. Uninfected cells either failed to fill up the defects or formed fibrous tissue mainly composed of type I collagen. Excessive cells were partially dislocated to the joint margins, leading to osteophyte formation there if AdBMP-2-infected cells were used. These adverse effects, however, were not seen with AdIGF-1-infected cells.
Stimulation of perichondrium-derived mesenchymal cells by transfer of growth factor cDNA in a partial-thickness defect model allows for satisfactory cartilage restoration by a repair tissue comparable with hyaline articular cartilage.
研究细胞移植与生长因子互补脱氧核糖核酸(cDNA)转导相结合对大鼠关节软骨全层缺损的修复作用。
从肋软骨膜分离间充质细胞,在体外以携带骨形态发生蛋白2(BMP-2)或胰岛素样生长因子1(IGF-1)cDNA的腺病毒载体感染。将细胞悬浮于纤维蛋白胶中,应用于大鼠股骨髌沟机械诱导的关节软骨全层缺损处。对缺损填充情况进行定量分析,通过组织化学和免疫组织化学方法评估新形成组织的质量和整合情况。未感染细胞或感染LacZ报告基因载体的细胞作为对照。
移植细胞能够附着于受伤的关节软骨,且不会因关节活动而从缺损处移位。感染腺病毒载体AdBMP-2和AdIGF-1的细胞产生了透明形态的修复软骨,其富含蛋白聚糖的基质中Ⅱ型胶原阳性但Ⅰ型胶原阴性,在大多数缺损处恢复了关节表面。未感染细胞要么未能填充缺损,要么形成主要由Ⅰ型胶原组成的纤维组织。如果使用感染AdBMP-2的细胞,过多的细胞会部分移位至关节边缘,导致此处形成骨赘。然而,感染AdIGF-1的细胞未出现这些不良反应。
在关节软骨全层缺损模型中,通过生长因子cDNA转导刺激软骨膜来源的间充质细胞,可使修复组织形成与透明关节软骨相当的组织,从而实现令人满意的软骨修复。