Gagliardi Rachel, Koch Drew W, Loeser Richard, Schnabel Lauren V
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA.
Comparative Medicine Institute, North Carolina State University, Raleigh, North Carolina, USA.
J Orthop Res. 2025 Feb;43(2):292-303. doi: 10.1002/jor.26004. Epub 2024 Nov 1.
Osteoarthritis (OA) is a debilitating disease that impacts millions of individuals and has limited therapeutic options. A significant hindrance to therapeutic discovery is the lack of in vitro OA models that translate reliably to in vivo preclinical animal models. An alternative to traditional inflammatory cytokine models is the matrikine stimulation model, in which fragments of matrix proteins naturally found in OA tissues and synovial fluid, are used to stimulate cells of the joint. The objective of this study was to determine if matrikine stimulation of equine synovial fibroblasts and chondrocytes with fibronectin fragments (FN7-10) would result in an OA phenotype. We hypothesized that FN7-10 stimulation of equine articular cells would result in an OA phenotype with gene and protein expression changes similar to those previously described for human chondrocytes stimulated with FN7-10. Synovial fibroblasts and chondrocytes isolated from four horses were stimulated in monolayer culture for 6 or 18 h with 1 µM purified recombinant 42 kD FN7-10 in serum-free media. At the conclusion of stimulation, RNA was collected for targeted gene expression analysis and media for targeted protein production analysis. Consistent with our hypothesis, FN7-10 stimulation resulted in significant alterations to many important genes that are involved in OA pathogenesis including increased expression of IL-1β, IL-4, IL-6, CCL2/MCP-1, CCL5/RANTES, CXCL6/GCP-2, MMP-1, MMP-3, and MMP13. The results of this study suggest that the equine matrikine stimulation model of OA may prove useful for in vitro experiments leading up to preclinical trials.
骨关节炎(OA)是一种使人衰弱的疾病,影响着数百万人,且治疗选择有限。治疗发现的一个重大障碍是缺乏能够可靠转化为体内临床前动物模型的体外OA模型。传统炎症细胞因子模型的一种替代方法是基质因子刺激模型,在该模型中,OA组织和滑液中天然存在的基质蛋白片段被用于刺激关节细胞。本研究的目的是确定用纤连蛋白片段(FN7-10)刺激马滑膜成纤维细胞和软骨细胞是否会导致OA表型。我们假设,用FN7-10刺激马关节细胞会导致OA表型,其基因和蛋白质表达变化与先前用FN7-10刺激的人软骨细胞所描述的变化相似。从四匹马中分离出的滑膜成纤维细胞和软骨细胞在无血清培养基中用1µM纯化的重组42 kD FN7-10进行单层培养刺激6或18小时。刺激结束时,收集RNA用于靶向基因表达分析,收集培养基用于靶向蛋白质产生分析。与我们的假设一致,FN7-10刺激导致许多参与OA发病机制的重要基因发生显著改变,包括IL-1β、IL-4、IL-6、CCL2/MCP-1、CCL5/RANTES、CXCL6/GCP-2、MMP-1、MMP-3和MMP13的表达增加。本研究结果表明,马OA的基质因子刺激模型可能对临床前试验前的体外实验有用。