Evaluation of SUMO1 and POU2AF1 in whole blood from rheumatoid arthritis patients and at risk relatives. (25th January 2019)

• Record Type: Journal Article
• Authors: Romo‐García, Maria Fernanda; Nava‐Ramírez, Hilda Susana; Zapata‐Zúñiga, Martin; Macías‐Segura, Noe; Santiago‐Algarra, David; Castillo‐Ortiz, Jose Dionisio; Bastián, Yadira; Ramos‐Remus, Cesar; Enciso‐Moreno, Jose Antonio; Castañeda‐Delgado, Julio Enrique
• Is Part Of: International journal of immunogenetics. Volume 46:Number 2(2019:Apr.)
• Page Start: 59
• Page End: 66
• Publication Date: 2019-01-25
• Subjects: ACPA -- early rheumatoid arthritis -- first‐degree relatives -- POU2AF1 -- SUMO1; Immunogenetics -- Periodicals; 571.9648
• DOI: 10.1111/iji.12414
• Languages: English
• ISSNs: 1744-3121

Abstract

Abstract: Rheumatoid arthritis (RA) is a systemic autoimmune disorder characterized by chronic and symmetrical inflammation of synovial tissue with subsequent joint destruction. SUMO1 is an important regulator of apoptosis through non‐canonical mechanism in synovial fibroblasts, and POU2AF1 is a known B‐cell transcriptional co‐activator. The specific objective of this study was to measure the expression of SUMO1 and POU2AF1 on first‐degree relatives of patients with RA and also in the preclinical and clinical stages of RA and describe their possible role in RA physiopathology. Blood samples were collected from ACPA+, ACPA‐, early and established RA subjects recruited. ACPAs and CarP autoantibodies were determined by ELISA Eurodiagnostica CCplus kit according to previously described protocols. RNA was isolated from blood samples; the purity as integrity was determined. Gene expression analysis was made by RT‐qPCR using specific primers for SUMO1 and POU2AF1 mRNAs; relative expression was determined according to the 2 ‐ΔΔct method procedure. Significant differences in the expression of both, SUMO1 and POU2AF1 were identified when comparing arthritis versus healthy or ACPA+ individuals, suggesting that the down regulation of such genes starts after the onset of symptoms in RA patients. Also, a significant correlation was identified for POU2AF1 and disease progression whit a downward trend for those with established RA. The implications of such gene down regulation are discussed in the context of RA physiopathology.