MSRA polymorphism is associated with the risk of rheumatoid arthritis in a Chinese population
1Department of Ophthalmology, Affiliated Hospital of Suzhou University, Changzhou No. 4 People's Hospital, Changzhou, China.
Objectives:
The expression of receptor activator of methionine sulfoxide reductase A (MSRA) and that of receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) are closely related to rheumatoid arthritis (RA). Our aim was to confirm whether MSRA and RANKL polymorphisms play a role in RA in a Chinese population.
Methods:
We investigated the presence of MSRA rs10903323 G/A and RANKL rs7984870 C/G polymorphisms in 329 patients with RA and 697 controls in a Chinese population. Genotyping was performed using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS).
Results:
When the MSRA rs10903323 GG homozygote genotype was used as the reference group, the GA genotype was associated with a significantly increased risk for RA. In the dominant model, when the MSRA rs10903323 GG homozygote genotype was used as the reference group, the GA/AA genotypes were associated with a significantly increased susceptibility to RA. The RANKL rs7984870 C/G polymorphism was not associated with a risk for RA. In stratification analyses, a significantly increased risk for RA associated with the MSRA rs10903323 GA genotype was evident among male patients, older patients, C-reactive protein (CRP)-positive patients, and anti-cyclic citrullinated peptide (anti-CCP) negative patients compared with the MSRA rs10903323 GG genotype.
Conclusions:
These findings suggest that the MSRA rs10903323 G/A variant allele is associated with RA development, especially among male patients, older patients, CRP-positive patients, and anti-CCP negative patients.
Insights
The MSRA rs10903323 G/A polymorphism increases rheumatoid arthritis (RA) risk in the Chinese population. This genetic variant is particularly associated with RA development in male, older, CRP-positive, and anti-CCP-negative patients.
Area of Science:
- Genetics
- Rheumatology
- Immunology
Background:
- Rheumatoid arthritis (RA) is an autoimmune disease with complex genetic factors.
- Receptor activator of methionine sulfoxide reductase A (MSRA) and receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) are implicated in RA pathogenesis.
- Understanding the role of genetic polymorphisms in RA susceptibility is crucial for diagnosis and treatment.
Purpose of the Study:
- To investigate the association between MSRA rs10903323 G/A and RANKL rs7984870 C/G polymorphisms and rheumatoid arthritis (RA) risk in a Chinese population.
- To determine if specific genotypes of MSRA and RANKL are linked to increased susceptibility to RA.
- To explore potential correlations between these polymorphisms and clinical characteristics of RA patients.
Main Methods:
- A case-control study involving 329 RA patients and 697 healthy controls from a Chinese population.
- Genotyping of MSRA rs10903323 G/A and RANKL rs7984870 C/G polymorphisms using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS).
- Statistical analysis to assess the association between genotypes and RA risk, including stratification by gender, age, CRP, and anti-CCP status.
Main Results:
- The MSRA rs10903323 G/A polymorphism was significantly associated with an increased risk of RA.
- Specifically, the GA genotype and the GA/AA genotypes (dominant model) showed increased susceptibility to RA.
- No significant association was found between the RANKL rs7984870 C/G polymorphism and RA risk.
- Stratification analysis revealed that the MSRA rs10903323 GA genotype conferred a higher RA risk in male, older, CRP-positive, and anti-CCP-negative individuals.
Conclusions:
- The MSRA rs10903323 G/A variant allele is a risk factor for rheumatoid arthritis (RA) development in the Chinese population.
- This genetic association is particularly pronounced in specific subgroups, including males, older individuals, and those who are CRP-positive and anti-CCP-negative.
- The findings highlight the potential role of MSRA gene polymorphisms in RA pathogenesis and suggest the need for further research into targeted genetic screening.
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