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 Detalle_Publicacion

Association study of MIA3 rs17465637 polymorphism with cardiovascular disease in rheumatoid arthritis patients

Abstract: Rheumatoid arthritis (RA) is a complex polygenic inflammatory disease associated with accelerated atherosclerosis. Melanoma inhibitor protein 3 (MIA3) is required for the export of collagen VlI (COL7A1) from the endoplasmic reticulum and it appears to be a tumor suppressor of malignant melanoma. Genome-wide association studies have described an association between MIA3 rs17465637 A/C polymorphisms and coronary artery disease and myocardial infarction. Because of that, we assessed the MIA3 rs17465637 polymorphism in 1505 RA Spanish patients stratified according to the presence/absence of cardiovascular (CV) disease. Also, a subgroup of patients without CV events was assessed for the presence of subclinical atherosclerosis using carotid ultrasound to establish carotid intima-media wall thickness and carotid plaques and brachial ultrasonography to determine the presence of endothelial dysfunction by flow-mediated endothelium-dependent and independent vasodilatation. MIA3 rs17465637 allele A showed a trend for association with the presence of carotid plaques (odds ratio 1.56, 95% confidence interval [0.96?2.51]; p=0.07). However, apart from an association of the MIA3 rs17465637 A allele with the risk of CV events in RA patients with dyslipidemia (p=0.018), no other significant associations were found between the presence of MIA3 rs17465637 A allele and the risk of suffering CV events or other surrogate markers of atherosclerosis. In conclusion, our results suggest a potential association of the MIA3 rs17465637 with CV disease in dyslipidemic patients with RA. However, additional studies are required to better establish the role of the MIA3 gene in mechanisms leading to the accelerated atherogenesis observed in RA. Many distinct inflammatory pathways contribute to the autoimmune disease rheumatoid arthritis and many patients have co-morbidities that may be associated with the same underlying mutations or regulatory defects.

 Autoría: García-Bermúdez M., López-Mejías R., González-Juanatey C., Corrales A., Castañeda S., Miranda-Filloy J.A., Gómez-Vaquero C., Fernández-Gutiérrez B., Balsa A., Pascual-Salcedo D., Blanco R., González-Álvaro I., Llorca J., Martín J., González-Gay M.A.,

 Fuente: DNA and Cell Biology, 2012, 31:8, 1412-1417

Editorial: Mary Ann Liebert

 Año de publicación: 2012

Nº de páginas: 6

Tipo de publicación: Artículo de Revista

 DOI: 10.1089/dna.2012.1672

ISSN: 1044-5498,1557-7430

Url de la publicación: https://doi.org/10.1089/dna.2012.1672

Autoría

GARCÍA-BERMÚDEZ, MERCEDES

RAQUEL LOPEZ MEJIAS

GONZÁLEZ-JUANATEY, CARLOS

ALFONSO FERNANDO CORRALES MARTINEZ

SANTOS CASTAÑEDA SANZ

MIRANDA-FILLOY, JOSÉ A.

GÓMEZ-VAQUERO, CARMEN

FERNÁNDEZ-GUTIÉRREZ, BENJAMÍN

BALSA, ALEJANDRO

PASCUAL-SALCEDO, DORA

GONZÁLEZ-ÁLVARO, ISIDORO

FRANCISCO JAVIER LLORCA DIAZ

MARTÍN, JAVIER