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MiR-548aj-3p and miR-3127-3p suppress RANKL-facilitated inflammatory cytokines and catabolic factor in osteoarthritis and rheumatoid arthritis

ABSTRACT: Osteoarthritis (OA) and rheumatoid arthritis (RA) are high prevalent joint diseases in global. The common pathological features include synovial inflammation, swelling, joint destruction, and bone remodelling. Arthritis development is associated with joint inflammation, particularly in inflamed synovial cells. Synovial inflammation, driven by cytokines such as interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), is a crucial factor in arthritis as it contributes to joint destruction. RANKL is a vital factor that is linked to the activity of osteoclasts and the erosion of bone. Increased levels of RANKL related with the proinflammatory cytokines and cartilage degradation enzymes expression, playing a role in the course of arthritis. Medicines for arthritis have been limited by side effects and individual variability in therapeutic response. More effective treatment and drug options are needed to improve disease progression. miRNAs directly modulate gene transcription as potential option for arthritis therapeutic. Our study revealed that RANKL stimulation in OA and RA synovial fibroblasts upregulated the expression of IL-1β, IL-6 (pro-inflammatory cytokines) and MMP-13 (catabolic factor) by suppressing miR-548aj-3p and miR-3127-3p. Administration of miR-548aj-3p and miR-3127-3p mimics substantially inhibited the expression of IL-1β, IL-6 and MMP-13. We propose a potentially efficacious miRNA therapeutic approach for the treatment of arthritis, with a specific focus on OA and RA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE281545 | GEO | 2025/11/30

REPOSITORIES: GEO

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Project description:Rheumatoid arthritis (RA) is an inflammatory joint disorder that results in progressive joint damage when insufficiently treated. In order to prevent joint destruction and functional disability in RA, early diagnosis and initiation of appropriate treatment with Disease-Modifying Antirheumatic Drugs (DMARDs) is needed. However, in daily clinical practice, patients may initially display symptoms of arthritis that do not fulfil the classification criteria for a definite diagnosis of RA, or any other joint disease, a situation called “Undifferentiated Arthritis” (UA). Out of the patients with UA, 30 to 50% usually develop RA, and early identification of these remains a challenge. At the present time, although several risk factors associated with the development of RA have been identified (6-9), a model that reliably predicts the probability of evolution of UA into RA in individual patients is lacking. In order to better identify early RA patients, an American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) collaboration recently developed new classification criteria. Although these criteria are more sensitive, the risk of over-diagnosis is an important issue to consider, especially in very early disease. In this context, the present study explores the feasibility of a molecular diagnosis of arthritis, based on the identification of disease-specific transcriptomic profiles in synovial biopsies from patients with arthritis according to the underlying condition. In a previous study, we performed global analyses of gene expression in synovial biopsies from patients with RA, Systemic Lupus Erythematosus (SLE) and Osteoarthritis (OA), using high-density oligonucleotide spotted microarrays. We found that the gene expression profiles are strikingly different according to the underlying condition. Thus, the majority of the genes up-regulated in SLE are type I Interferon-inducible genes, as compared with the up-regulation genes involved in T cell and B cell activation in RA, and in extracellular matrix homeostasis in OA. Based on these results, similar analyses were performed in synovial biopsies from patients with seronegative arthritis (SA) and microcrystalline arthritis (MIC), in order to identify disease-specific molecular signatures.

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MiR-548aj-3p and miR-3127-3p suppress RANKL-facilitated inflammatory cytokines and catabolic factor in osteoarthritis and rheumatoid arthritis

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