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LncRNA MEG3 as a biomarker and therapeutic target in rheumatoid arthritis: Insights from gene polymorphisms,
Sha-Sha Tao1, Hai-Fen Wei2, Shu-Zhen Xu2
1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, People's Republic of China; Experimental Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, Hefei, Anhui, China.
Abstract:
Maternally expressed gene 3 (MEG3) is implicated in autoimmunity, but its role in rheumatoid arthritis (RA) is unclear. This study aimed to investigate gene polymorphisms, expression patterns, and functional mechanisms of MEG3 in RA pathogenesis and its clinical associations. MEG3 single nucleotide polymorphisms (SNPs) were genotyped in 551 RA patients and 595 controls, finding no association with RA susceptibility. MEG3 expression was downregulated in peripheral blood mononuclear cells (PBMCs) from RA patients, particularly in ACPA-positive cases, but increased with NSAID use. In fibroblast-like synoviocytes (FLS), MEG3 was downregulated. Overexpression of MEG3 inhibited FLS proliferation and invasion, lowering IL-1β and IL-6 but not TNF-α. Whereas MEG3 knockdown enhanced FLS proliferation and invasion, elevating TNF-α and IL-1β without altering IL-6. Collectively, MEG3 polymorphisms are not associated with RA susceptibility. MEG3 dysregulation correlates with RA clinical indicators and regulates FLS pathogenicity, indicating its potential as a clinical biomarker and therapeutic target in RA.
Insights
Maternally expressed gene 3 (MEG3) is not linked to rheumatoid arthritis (RA) susceptibility. However, MEG3 dysregulation in RA affects fibroblast-like synoviocytes, suggesting its potential as a biomarker and therapeutic target.
Area of Science:
- Immunology
- Genetics
- Molecular Biology
Background:
- Maternally expressed gene 3 (MEG3) is linked to autoimmune diseases, but its specific role in rheumatoid arthritis (RA) remains largely unknown.
- Understanding the genetic and functional aspects of MEG3 in RA is crucial for identifying new therapeutic strategies.
Purpose of the Study:
- To investigate the association of MEG3 gene polymorphisms with RA susceptibility.
- To analyze MEG3 expression patterns in RA patients and their correlation with clinical features.
- To elucidate the functional role of MEG3 in the pathogenesis of RA, particularly in fibroblast-like synoviocytes (FLS).
Main Methods:
- Genotyping of MEG3 single nucleotide polymorphisms (SNPs) in 551 RA patients and 595 healthy controls.
- Quantitative analysis of MEG3 expression in peripheral blood mononuclear cells (PBMCs) and FLS from RA patients.
- In vitro experiments involving MEG3 overexpression and knockdown in FLS to assess its impact on cell proliferation, invasion, and cytokine production (IL-1β, IL-6, TNF-α).
Main Results:
- No significant association was found between MEG3 SNPs and RA susceptibility.
- MEG3 expression was significantly downregulated in PBMCs of RA patients, especially in anti-citrullinated protein antibody (ACPA)-positive cases, and this downregulation was partially reversed by NSAID use.
- MEG3 downregulation in FLS correlated with increased FLS proliferation and invasion, accompanied by altered secretion of pro-inflammatory cytokines (IL-1β, TNF-α).
- Overexpression of MEG3 suppressed FLS proliferation and invasion while reducing IL-1β and IL-6 levels.
Conclusions:
- MEG3 gene polymorphisms do not contribute to RA susceptibility.
- MEG3 dysregulation is a feature of RA pathogenesis and is associated with disease activity and FLS behavior.
- MEG3 holds potential as a biomarker for RA and a therapeutic target for managing RA-related inflammation and joint destruction.
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