Synovial Fluid Laboratory, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Calzada Mexico-Xochimilco 289, Col. Arenal de Guadalupe, Tlalpan, 14389, Mexico City, Mexico.
Facultad de Medicina, Universidad Autónoma de Guadalajara, Guadalajara, Jalisco, Mexico.
Mol Biol Rep. 2020 Apr;47(4):2627-2634. doi: 10.1007/s11033-020-05351-4. Epub 2020 Mar 5.
Articular cartilage is an avascular tissue with a structure that allows it to support and cushion the overload of the surfaces in contact. It maintains its metabolic functions due to the contribution of different signaling pathways. However, several factors play a role in its deterioration, allowing to the development of osteoarthritis (OA), and one of the major factors is genetic. Our goal was to identify gene-gene interactions (epistasis) between five signaling pathways involved in the articular cartilage metabolism as possible indicators of OA risk. We applied the Multifactor-Dimensionality Reduction (MDR) method to identify and characterize the epistasis between 115 SNPs located in 73 genes related to HIF-1α, Wnt/β-catenin, cartilage extracellular matrix metabolism, oxidative stress, and uric acid transporters. Ninety three patients diagnosed with primary knee OA and 150 healthy controls were included in the study. Genotyping was performed with the OpenArray system, the statistical analysis was carried out with the STATA software v14, and epistasis was analyzed with the MDR software v3.0.2. The MDR analysis revealed that the best interaction model was between polymorphisms rs17786744 of the STC1 gene and rs2615977 of the COL11A1 gene, with an entropy value of 4.44%, CVC 8/10, OR 5.60, 95% CI 3.27-9.59, p < 0.0001. Under this interaction model, we identified high and low risk genotypes involved in OA development. Our results suggest complex interactions between STC1 and COL11A1 genes that might have an impact on genetic susceptibility to develop OA. Further studies are required to confirm it.
关节软骨是一种无血管组织,其结构使其能够支撑和缓冲接触表面的超负荷。它通过不同信号通路的贡献维持其代谢功能。然而,有几个因素在其恶化中起作用,导致骨关节炎(OA)的发展,其中一个主要因素是遗传。我们的目标是确定参与关节软骨代谢的五个信号通路之间的基因-基因相互作用(上位性),作为 OA 风险的可能指标。我们应用多因子降维(MDR)方法来识别和描述位于与 HIF-1α、Wnt/β-catenin、软骨细胞外基质代谢、氧化应激和尿酸转运体相关的 73 个基因中的 115 个 SNP 之间的上位性。93 名被诊断为原发性膝骨关节炎的患者和 150 名健康对照者被纳入研究。采用 OpenArray 系统进行基因分型,使用 STATA 软件 v14 进行统计分析,使用 MDR 软件 v3.0.2 进行上位性分析。MDR 分析显示,最佳互作模型是 STC1 基因 rs17786744 多态性与 COL11A1 基因 rs2615977 之间的多态性,熵值为 4.44%,CVC 8/10,OR 5.60,95%CI 3.27-9.59,p<0.0001。在这种互作模型下,我们确定了与 OA 发展相关的高风险和低风险基因型。我们的结果表明,STC1 和 COL11A1 基因之间存在复杂的相互作用,可能对遗传易感性产生影响。需要进一步的研究来证实这一点。