DuRaine Grayson, Neu Corey P, Chan Stephanie M T, Komvopoulos Kyriakos, June Ronald K, Reddi A Hari
Center for Tissue Regeneration and Repair, Department of Orthopaedic Surgery, University of California, Davis, Medical Center, Sacramento, CA 95817, USA.
J Orthop Res. 2009 Feb;27(2):249-56. doi: 10.1002/jor.20713.
Articular cartilage functions to provide a low-friction surface for joint movement for many decades of life. Superficial zone protein (SZP) is a glycoprotein secreted by chondrocytes in the superficial layer of articular cartilage that contributes to effective boundary lubrication. In both cell and explant cultures, TGF-beta1 and IL-1beta have been demonstrated to, respectively, upregulate and downregulate SZP protein levels. It was hypothesized that the friction coefficient of articular cartilage could also be modulated by these cytokines through SZP regulation. The friction coefficient between cartilage explants (both untreated and treated with TGF-beta1 or IL-1beta) and a smooth glass surface due to sliding in the boundary lubrication regime was measured with a pin-on-disk tribometer. SZP was quantified using an enzyme-linked immunosorbant assay and localized by immunohistochemistry. Both TGF-beta1 and IL-1beta treatments resulted in the decrease of the friction coefficient of articular cartilage in a location- and time-dependent manner. Changes in the friction coefficient due to the TGF-beta1 treatment corresponded to increased depth of SZP staining within the superficial zone, while friction coefficient changes due to the IL-1beta treatment were independent of SZP depth of staining. However, the changes induced by the IL-1beta treatment corresponded to changes in surface roughness, determined from the analysis of surface images obtained with an atomic force microscope. These findings demonstrate that the low friction of articular cartilage can be modified by TGF-beta1 and IL-1beta treatment and that the friction coefficient depends on multiple factors, including SZP localization and surface roughness.
关节软骨的功能是在数十年的生命过程中为关节运动提供低摩擦表面。表层区蛋白(SZP)是一种由关节软骨表层的软骨细胞分泌的糖蛋白,有助于实现有效的边界润滑。在细胞培养和组织块培养中,已证实转化生长因子β1(TGF-β1)和白细胞介素1β(IL-1β)分别上调和下调SZP蛋白水平。据推测,这些细胞因子也可通过调节SZP来调节关节软骨的摩擦系数。使用销盘摩擦磨损试验机测量了在边界润滑状态下滑动时,软骨组织块(未处理以及用TGF-β1或IL-1β处理)与光滑玻璃表面之间的摩擦系数。使用酶联免疫吸附测定法定量SZP,并通过免疫组织化学进行定位。TGF-β1和IL-1β处理均导致关节软骨摩擦系数以位置和时间依赖性方式降低。TGF-β1处理引起的摩擦系数变化与表层区内SZP染色深度增加相对应,而IL-1β处理引起的摩擦系数变化与SZP染色深度无关。然而,IL-1β处理引起的变化与表面粗糙度的变化相对应,表面粗糙度是通过分析原子力显微镜获得的表面图像确定的。这些发现表明,TGF-β1和IL-1β处理可改变关节软骨的低摩擦,且摩擦系数取决于多种因素,包括SZP定位和表面粗糙度。