Background Patients with rheumatoid arthritis (RA) tend to have higher incidence of atherosclerosis and the chances of stroke or myocardial infarction also increase significantly in those patients. CD36 is responsible for the major part of oxidized low-density lipoprotein (ox-LDL) uptake by macrophages, suggesting atherogenic properties for CD36. Advanced glycation end products (AGEs) are a heterogeneous group of substances formed by the nonenzymatic glycation in serum and tissues. Matrix metalloproteinases (MMPs) are responsible for the degradation of most extracellular matrix proteins and mediate tissue remodeling in a variety of pathologic conditions.
Objectives The aim of this study was to identify CD36 mRNA expression and to determine its association with the circulating levels of AGEs and MMPs in patients with RA.
Methods A total of 60 subjects, including thirty patients with RA and thirty healthy subjects participated in this study. Peripheral blood mononuclear cell RNA was used to analyze the CD36 mRNA expression by RT-PCR. Plasma concentrations of the AGEs, ox-LDL, receptor for AGEs (RAGE), interleukin-17 (IL-17), matrix metalloproteinases-2 (MMP-2), MMP-9, tissue inhibitor of metalloproteinases-1 (TIMP-1), and TIMP-2 were determined by enzyme-linked immunosorbent assay.
Results CD36 mRNA expression in RA patients was significantly lower than healthy subjects. AGEs and MMP-9 concentrations of RA patients were significantly higher but RAGE levels were significantly lower than those in healthy subjects. RA patients have increased ox-LDL levels along with increased cardiovascular risk. In RA patients, plasma AGEs concentration positively correlated with fasting insulin, TC/HDL-C, and IL-17, whereas ox-LDL concentration positively related to MMP-2 and TC/HDL-C.
Conclusions RA patients have reduced CD36 mRNA expression and decreased RAGE along with abnormal levels of AGEs and MMPs, suggesting the risk of atherosclerosis in RA patients may at least in part relate to interaction of glycation, oxidation, and MMP function.
Disclosure of Interest None Declared