Uncoupling Protein 2 as genetic risk factor for systemic lupus erythematosus: association with malondialdehyde levels and intima media thickness
- Autori: Caterina M. GAMBINO, Giulia ACCARDI, Anna AIELLO, Calogero CARUSO, Ciriaco CARRU, Bruno G. GIOIA, Giuliana GUGGINO, Sergio RIZZO, Angelo ZINELLU, Marcello CIACCIO, Giuseppina CANDORE
- Anno di pubblicazione: 2020
- Tipologia: Articolo in rivista
- OA Link: http://hdl.handle.net/10447/450844
vascular diseases, the main cause of death in systemic lupus erythematous (SLE ). To gain insight into these mechanisms, we studied the association of uncoupling protein (UCP) 2 genetic variants, gene involved in the mitochondrial production of reactive oxygen species, and oxidative stress with SLE and the presence of atherosclerosis. METHOD S: Genetic analysis of the UCP2 -866G/A and UCP2 Ins/Del polymorphisms was performed in 45 SLE patients and 36 healthy controls by RFLP-PCR. Oxidation status was determined by measuring malondialdehyde (MDA ) levels. Presence of subclinical atherosclerosis was investigated by evaluation of intima-media thickness using echo-color-Doppler carotid ultrasound examination. RESULTS: Allelic and genotypic frequencies of the SNPs analysed were evaluated by gene count. Significant association was found between UCP2-866A allele and susceptibility for SLE (P=0.001). Higher levels of MDA were found significantly increased in SLE patients (MDA , 5.05±3.36 μmol/L) compared to normal controls (MDA , 2.79±0.89 μmol/L) (P<0.0001). CONCLUSIO NS: Our results suggest that -866G/A UCP2 polymorphism is associated with SLE causing increased RO S production that, in turn, results in increased MDA levels responsible of accelerated atherosclerosis.