Comparative Analysis Revealed Circulating Methylation of PDGFRB Highly Related with Rheumatoid Arthritis Related Diseases.

Abstract

Introduction: To investigate the DNA methylation levels of platelet-derived growth factor receptor- B [PDGFRB] cg25613180 across rheumatoid arthritis [RA] and various further rheumatic disorders, including ankylosing spondylitis [AS], psoriatic arthritis [PsA], gouty arthritis, systemic lupus erythematosus [SLE], sjögren's syndrome [SS], and dermatomyositis [DM], using targeted DNA methylation sequencing.

Methods: Methylation levels at PDGFRB cg25613180 were assessed in a cohort comprising RA patients, healthy controls [HC], and individuals diagnosed with AS, PsA, gout, SLE, SS, and DM. Pearson- 's correlation analysis was conducted to explore the relationship between PDGFRB cg25613180 methylation levels and key clinical indices associated with RA. Additionally, both univariate and multivariate logistic regression analyses were performed to evaluate the potential of methylation status as a diagnostic biomarker for RA.

Results: Patients with RA demonstrated notably lower PDGFRB cg25613180 methylation levels than the HCs, with similar trends noted in the SLE and DM teams. Methylation levels are negatively correlated with inflammatory indicators like C-reactive protein [CRP], along with erythrocyte sedimentation rate [ESR] in RA. Differences in haplotype methylation were also significant between the RA and other groups, particularly for the CCCC and TCCC haplotypes. The logistic regression model provided high discriminative accuracy between RA and other conditions, particularly AS.

Discussion: The results indicate that PDGFRB methylation, particularly at cg25613180, exhibits distinct patterns in RA compared to other rheumatic diseases. This suggests its potential as a diagnostic biomarker for RA. The negative correlation with inflammatory markers suggests a role for PDGFRB methylation in the inflammatory processes underlying RA. The study also highlights the utility of haplotype- specific methylation analysis in enhancing diagnostic accuracy.

Conclusion: This study identifies distinct PDGFRB methylation patterns in RA, supporting its potential as a biomarker for diagnosis and differentiation from other rheumatic diseases. The findings open avenues for further exploration of PDGFRB methylation in understanding the epigenetic landscape of autoimmune rheumatic diseases and their potential for clinical applications.