Fu Sai-Chuen, Wong Yim-Ping, Cheuk Yau-Chuk, Lee Kwong-Man, Chan Kai-Ming
Department of Orthopaedics & Traumatology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong.
Clin Orthop Relat Res. 2005 Feb(431):226-32. doi: 10.1097/01.blo.0000145887.48534.6f.
Transforming growth factor-beta1 is known for its effect on the production of extracellular matrix in tendons. Elevated levels of transforming growth factor-beta1 have been reported in tendon adhesion and tendinosis, which suggests that transforming growth factor-beta1 plays an important role in matrix disturbances. Tendon adhesion involves excessive collagen deposition, whereas tendinosis is associated with increased proteoglycan deposition. It seems that other factors also may affect matrix deposition and modulate the effects of transforming growth factor-beta1. We assessed whether matrix anchorage to Type I collagen or fibronectin could change the gene expression of matrix proteins in tendon fibroblasts, and studied whether the effects of transforming growth factor-beta1 were altered by matrix anchorage. Human patellar tendon fibroblast cultures were prepared in different cell anchorages, and the cellular responses to transforming growth factor-beta1 were measured as gene expression of procollagen Type I, Type III, decorin, and biglycan by real-time reverse transcriptase-polymerase chain reaction. Fibronectin anchorage significantly increased the messenger ribonucleic acid level of decorin, and the messenger ribonucleic acid level of procollagen Type I was decreased by matrix anchorage to either fibronectin or Type I collagen. Transforming growth factor-beta1 increased the messenger ribonucleic acid level of procollagen Type I in Type I collagen-coated plates, but it suppressed the messenger ribonucleic acid level of decorin in fibronectin-coated plates. These findings suggest that interaction of matrix anchorage and transforming growth factor-beta1 is an important determinant of matrix deposition in healing tendons and the development of matrix disturbances in tendons.
转化生长因子-β1因其对肌腱中细胞外基质产生的影响而闻名。在肌腱粘连和肌腱病中已报道转化生长因子-β1水平升高,这表明转化生长因子-β1在基质紊乱中起重要作用。肌腱粘连涉及过多的胶原蛋白沉积,而肌腱病与蛋白聚糖沉积增加有关。似乎其他因素也可能影响基质沉积并调节转化生长因子-β1的作用。我们评估了基质与I型胶原蛋白或纤连蛋白的锚定是否会改变肌腱成纤维细胞中基质蛋白的基因表达,并研究了基质锚定是否会改变转化生长因子-β1的作用。在不同的细胞锚定下制备人髌腱成纤维细胞培养物,并通过实时逆转录聚合酶链反应测量细胞对转化生长因子-β1的反应,以I型、III型前胶原、核心蛋白聚糖和双糖链蛋白聚糖的基因表达作为指标。纤连蛋白锚定显著增加了核心蛋白聚糖的信使核糖核酸水平,而基质与纤连蛋白或I型胶原蛋白的锚定均降低了I型前胶原的信使核糖核酸水平。在I型胶原蛋白包被的培养板中,转化生长因子-β1增加了I型前胶原的信使核糖核酸水平,但在纤连蛋白包被的培养板中,它抑制了核心蛋白聚糖的信使核糖核酸水平。这些发现表明,基质锚定与转化生长因子-β1的相互作用是愈合肌腱中基质沉积和肌腱基质紊乱发展的重要决定因素。