RESUMEN
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.
Asunto(s)
Artritis Reumatoide/sangre , Familia , Proteína SUMO-1/sangre , Transactivadores/sangre , Adulto , Artritis Reumatoide/genética , Regulación hacia Abajo/genética , Femenino , Redes Reguladoras de Genes , Humanos , Masculino , ARN Mensajero/genética , ARN Mensajero/metabolismo , Factores de Riesgo , Proteína SUMO-1/genética , Transactivadores/genéticaRESUMEN
Alzheimer's disease (AD) is the most common type of dementia in the elderly. The accumulation of amyloid-ß peptides and tau proteins is the major pathogenic event of AD. There is accumulating evidence that both tau and amyloid-ß linked to the small ubiquitin-like modifier (SUMO), which is increased in the brain of AD model mouse. The present study focused on the determination of SUMO1 protein level in AD blood plasma by the ELISA methods. We compared plasma from 80 dementia patients (average age 75.3 y), 89 persons with amnestic mild cognitive impairment (MCI) (average age 73.71 y),and 133 cognitively normal controls (average age 71.97 y). The plasma level of SUMO1 was significantly increased in dementia patients, as compared to control groups. The levels of SUMO1 correlated to decreased Mini-Mental State Examination (râ=-0.123, pâ=â0.029). These results suggest that elevated plasma SUMO1 levels may be associated with AD.
