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Association of UCP2 - 866 G/A polymorphism with chronic inflammatory diseases
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
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2009 (English)In: Genes and Immunity, ISSN 1466-4879, E-ISSN 1476-5470, Vol. 10, no 6, 601-605 p.Article in journal (Refereed) Published
Abstract [en]

We reported earlier that two mitochondrial gene polymorphisms, UCP2 -866 G/A (rs659366) and mtDNA nt13708 G/A (rs28359178), are associated with multiple sclerosis (MS). Here we aim to investigate whether these functional polymorphisms contribute to other eight chronic inflammatory diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Wegener' granulomatosis (WG), Churg-Strauss syndrome (CSS), Crohn's disease (CD), ulcerative colitis (UC), primary sclerosing cholangitis (PSC) and psoriasis. Compared with individual control panels, the UCP2 -866 G/A polymorphism was associated with RA and SLE, and the mtDNA nt13708 G/A polymorphism with RA. Compared with combined controls, the UCP2 -866 G/A polymorphism was associated with SLE, WG, CD and UC. When all eight disease panels and the original MS panel were combined in a meta-analysis, the UCP2 was associated with chronic inflammatory diseases in terms of either alleles (odds ratio (OR)=0.91, 95% confidence interval (95% CI): 0.86-0.96), P=0.0003) or genotypes (OR=0.88, (95% CI: 0.82-0.95), P=0.0008), with the -866A allele associated with a decreased risk to diseases. As the -866A allele increases gene expression, our findings suggest a protective role of the UCP2 protein in chronic inflammatory diseases.

Place, publisher, year, edition, pages
2009. Vol. 10, no 6, 601-605 p.
Keyword [en]
mitochondria, chronic inflammatory diseases, uncoupling protein 2
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-111978DOI: 10.1038/gene.2009.29ISI: 000269493400008PubMedID: 19387457OAI: oai:DiVA.org:uu-111978DiVA: diva2:284214
Available from: 2010-01-08 Created: 2010-01-05 Last updated: 2017-12-12Bibliographically approved

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Alarcón-Riquelme, Marta E.

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