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ORIGINAL ARTICLE  MECHANISTIC FACTORS OF CARDIOVASCULAR DISEASES: FOCUS ON PREVENTION AND TREATMENT 

Minerva Cardioangiologica 2020 December;68(6):609-18

DOI: 10.23736/S0026-4725.20.05225-1

Copyright © 2020 EDIZIONI MINERVA MEDICA

lingua: Inglese

Uncoupling Protein 2 as genetic risk factor for systemic lupus erythematosus: association with malondialdehyde levels and intima media thickness

Caterina M. GAMBINO 1, Giulia ACCARDI 1, Anna AIELLO 1, Calogero CARUSO 1, Ciriaco CARRU 2, Bruno G. GIOIA 1, Giuliana GUGGINO 3, Sergio RIZZO 4, Angelo ZINELLU 2, Marcello CIACCIO 1, Giuseppina CANDORE 1

1 Department of Biomedicine, Neurosciences and Advanced Diagnostics, University of Palermo, Palermo, Italy; 2 Department of Biomedical Sciences, University of Sassari, Sassari, Italy; 3 Unit of Rheumatology, Paolo Giaccone University Hospital, Palermo, Italy; 4 Unit of Transfusion Medicine, Paolo Giaccone University Hospital, Palermo, Italy



BACKGROUND: Increased oxidative stress potentially leads to accelerated atherosclerosis and, consequently, cardiovascular 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.
METHODS: 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).
CONCLUSIONS: Our results suggest that -866G/A UCP2 polymorphism is associated with SLE causing increased ROS production that, in turn, results in increased MDA levels responsible of accelerated atherosclerosis.


KEY WORDS: Lupus erythematosus, systemic; Genetics; Cardiovascular diseases

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