Abstract
Osteoprotegerin (OPG), receptor activator of nuclear factor-ΚB ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have been involved in rheumatoid arthritis (RA) pathophysiology. In this study, we assessed messenger RNA (mRNA) expression of these molecules by qPCR in peripheral blood from 26 patients with RA (12 of them with ischemic heart disease –IHD) and 10 healthy controls. Correlation coefficients between OPG, RANKL and TRAIL expression levels in RA patients and their clinical and demographic characteristics were also evaluated. Whereas OPG and OPG/TRAIL ratio expression were significantly increased in RA patients compared to controls (fold change = 1.79, p = 0.013 and 2.07, p = 0.030, respectively), RANKL/OPG ratio was significantly decreased (fold change = 0.50, p = 0.020). No significant differences were found between patients and controls in RANKL and TRAIL expression. Interestingly, TRAIL expression was significantly higher in RA patients with IHD compared to those without IHD (fold change = 1.46, p = 0.033). Moreover, biologic disease-modifying antirheumatic drugs (DMARDs) significantly decreased RANKL expression in RA patients (p = 0.016). Our study supports an important role of OPG and TRAIL in RA. Furthermore, it highlights an effect of biologic DMARDs in the modulation of RANKL.
Highlights
Osteoprotegerin (OPG)/receptor activator of nuclear factor-ΚB ligand (RANKL)/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) system has been involved in the pathophysiology of rheumatoid arthritis (RA)[1,2]
No significant differences were found between patients and controls in RANKL and TRAIL messenger RNA (mRNA) expression (Table 1)
The OPG/ RANKL/TRAIL system has been linked to bone loss in RA and CV risk[1,6,8]
Summary
Osteoprotegerin (OPG)/receptor activator of nuclear factor-ΚB ligand (RANKL)/tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) system has been involved in the pathophysiology of rheumatoid arthritis (RA)[1,2]. OPG reduces RANKL-RANK interactions and inhibits osteoclastogenesis[3] In this regard, RANKL/OPG ratio plays an important role regulating bone homeostasis in RA, a disease characterized by bone and cartilage destruction[1,4]. It is well known that RA patients have an accelerated atherosclerotic process, leading to an increased risk of cardiovascular (CV) disease, including ischemic heart disease (IHD)[7]. In this sense, OPG/RANKL/TRAIL system has been related to atherosclerosis and CV disease[8]. Taking into account that both RA and CV disease are inflammatory systemic diseases, the assessment of OPG, RANKL and TRAIL expression at a systemic level (blood) is of main importance
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