Association of UCP2 −866 G A polymorphism with chronic inflammatory diseases
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, includin...
Saved in:
Published in | Genes and immunity Vol. 10; no. 6; pp. 601 - 605 |
---|---|
Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.09.2009
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | 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. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1466-4879 1476-5470 1476-5470 |
DOI: | 10.1038/gene.2009.29 |