类风湿性关节炎(RA)是一种复杂的自身免疫性疾病,可导致关节破坏。许多影响关节组织的免疫细胞参与了这种疾病的发病机理。这导致许多促炎介质的合成。毒品的运输,以及许多参与RA患者炎症发展的细胞因子,由膜转运蛋白介导。膜转运蛋白是介导底物跨生物膜转移的蛋白质。但是迄今为止,还没有研究检查关节组织中溶质载体(SLC)转运蛋白的表达。该研究的目的是评估RA患者滑膜(SMs)和髌下脂肪垫(Hoffa'spad)中单个SLC家族转运蛋白的表达。该研究包括20例类风湿关节炎患者和20例骨关节炎患者作为对照组,他们正在接受关节置换手术作为临床护理的正常部分。在RA患者的SM和Hoffa垫中,以下17种膜转运蛋白被定义为SLC转运蛋白超家族的相关表达水平:SLC15A2,SLC16A3,SLC19A1,SLC2A9,SLC22A1,SLC22A3,SLC22A4,SLC22A5,SLC22A18,SLC33A1,SLC47A1,SLC51A,SLC7A5、SLC7A6、SLC01C1、SLC02B1、SLC04A1。证实这些转运体在RA和OA患者的SM以及Hoffa垫中的表达,以及这些群体之间表达的差异,提示SLC转运体参与维持生理条件下关节组织的体内平衡,以及在RA的炎症过程中。
Rheumatoid arthritis (RA) is a complex autoimmune disease that leads to joint destruction. A number of immune cells that affect joint tissues are involved in the pathogenesis of this disease. This leads to the synthesis of many pro-inflammatory mediators. The transport of drugs, as well as many cytokines involved in the development of inflammation in RA patients, is mediated by membrane transporters. Membrane transporters are proteins that mediate the transfer of substrates across biological membranes. But to date there are no studies examining the expression of solute carrier (SLC) transporters in joint tissues. The aim of the study was to evaluate the expression of individual SLC family transporters in the synovial membranes (SMs) and infrapatellar fat pad (Hoffa\'s pad) of RA patients. The study included 20 patients with rheumatoid arthritis and 20 with osteoarthritis as the control group who were undergoing joint replacement surgery as a normal part of clinical care. In the SM and Hoffa\'s pad of RA patients the following 17 membrane transporters were defined at relevant expression levels for SLC transporter superfamily: SLC15A2, SLC16A3, SLC19A1, SLC2A9, SLC22A1, SLC22A3, SLC22A4, SLC22A5, SLC22A18, SLC33A1, SLC47A1, SLC51A, SLC7A5, SLC7A6, SLC01C1, SLC02B1, SLC04A1. The confirmed expression of these transporters in the SMs as well as Hoffa\'s pad of patients with RA and OA, and the differences in their expression between these groups, suggests the involvement of SLC transporters in both the maintenance of homeostasis under physiological conditions in the tissues of the joints, as well as in the inflammatory process in RA.