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Magnesium supplementation modifies synovial and splenic transcriptomic signatures and biologic pathways in arthritis mice

ABSTRACT: Rheumatoid arthritis (RA) is a common chronic autoimmune and inflammatory disease that can cause joint pain and disability. We have recently reported that oral magnesium supplementation significantly reduces disease severity and joint damage in two models of RA. In the synovial tissues. There was an enrichment for differentially expressed genes (DEGs) belonging to pathways implicated in transcription regulation, nuclear receptor signaling, and pathways implicated in RA pathogenesis such as RHO GTPases, RUNX1 pathway, oxidative stress induced senescence, senescence-associated secretory phenotype (SASP) and cell migration in synovial tissues . In the synovial tissues Actc1 and Nr4a3 were among the genes with the highest expression, while Krt79 and Ffar2 were among the genes with the most significantly decreased expression in Mg2800 group compared with Mg500. Spleens had an enrichment for Metabolism of folate and pterines, HSP90 chaperone cycle for steroid hormone receptor. Syt5 and Hspa1a were among the genes with the highest expression, while Ano2 and Ascl4 were among the genes with the lowest expression levels in spleens from Mg2800 compared with Mg500. We describe the tissue transcriptomic consequences of the arthritis-protecting increased Mg dietary intake in KSIA mice. These results show that oral Mg supplementation may interfere with pathways implicated response to oxidative stress and senescence, and other processes known to participate in RA pathogenesis. Our findings provide new evidence supporting the disease-suppressing effect of increased Mg intake in arthritis. Oral Mg supplementation has the potential to become a new addition to the therapeutic options for RA and other autoimmune and inflammatory diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE276773 | GEO | 2024/11/21

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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Magnesium supplementation modifies synovial and splenic transcriptomic signatures and biologic pathways in arthritis mice

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