Association of UCP2 -866 G/A polymorphism with chronic inflammatory diseases

X. Yu; S. Wieczorek; A. Franke; H. Yin; M. Pierer; C. Sina; T. H. Karlsen; K. M. Boberg; A. Bergquist; M. Kunz; T. Witte; W. L. Gross; J. T. Epplen; M. E. Alarcón-Riquelme; S. Schreiber; S. M. Ibrahim

doi:10.1038/gene.2009.29

Association of UCP2 -866 G/A polymorphism with chronic inflammatory diseases

X. Yu, S. Wieczorek, A. Franke, H. Yin, M. Pierer, C. Sina, T. H. Karlsen, K. M. Boberg, A. Bergquist, M. Kunz, T. Witte, W. L. Gross, J. T. Epplen, M. E. Alarcón-Riquelme, S. Schreiber, S. M. Ibrahim^*

^*Korrespondierende/r Autor/-in für diese Arbeit

88 Zitate (Scopus)

Abstract

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.

Originalsprache	Englisch
Zeitschrift	Genes and Immunity
Jahrgang	10
Ausgabenummer	6
Seiten (von - bis)	601-605
Seitenumfang	5
ISSN	1466-4879
DOIs	https://doi.org/10.1038/gene.2009.29
Publikationsstatus	Veröffentlicht - 2009

Fördermittel

The authors thank all patients, physicians and volunteer healthy controls for the cooperation. The cooperation of the Deutsche Morbus Crohn und Colitis Vereinigung e.V. and of the contributing gastroenterologists is gratefully acknowledged. The authors thank Rica Waterstadt for assistance in genotyping. This work was supported by grants from EU FP6 (EURO-RA), Hertie Stiftung, German Ministry of Education and Research (BMBF) through the National Genome Research Network (NGFN), Deutsche Forschungsgemeinschaft (KFO170) and the PopGen Biobank. The project received infrastructure support through the DFG excellence cluster ‘Inflammation at Interfaces’. Benedicte A Lie and the Norwegian Bone Marrow Donor Registry at Rikshospita- let University Hospital, Oslo, are acknowledged for contributing the healthy Norwegian control population.

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SDG 3 – Gesundheit und Wohlergehen

Strategische Forschungsbereiche und Zentren

Forschungsschwerpunkt: Infektion und Entzündung - Zentrum für Infektions- und Entzündungsforschung Lübeck (ZIEL)

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10.1038/gene.2009.29

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Yu, X., Wieczorek, S., Franke, A., Yin, H., Pierer, M., Sina, C., Karlsen, T. H., Boberg, K. M., Bergquist, A., Kunz, M., Witte, T., Gross, W. L., Epplen, J. T., Alarcón-Riquelme, M. E., Schreiber, S., & Ibrahim, S. M. (2009). Association of UCP2 -866 G/A polymorphism with chronic inflammatory diseases. Genes and Immunity, 10(6), 601-605. https://doi.org/10.1038/gene.2009.29

@article{2b3223c79dfd414a96b43397bd8effa3,

title = "Association of UCP2 -866 G/A polymorphism with chronic inflammatory diseases",

abstract = "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.",

author = "X. Yu and S. Wieczorek and A. Franke and H. Yin and M. Pierer and C. Sina and Karlsen, \{T. H.\} and Boberg, \{K. M.\} and A. Bergquist and M. Kunz and T. Witte and Gross, \{W. L.\} and Epplen, \{J. T.\} and Alarc{\'o}n-Riquelme, \{M. E.\} and S. Schreiber and Ibrahim, \{S. M.\}",

note = "Funding Information: The authors thank all patients, physicians and volunteer healthy controls for the cooperation. The cooperation of the Deutsche Morbus Crohn und Colitis Vereinigung e.V. and of the contributing gastroenterologists is gratefully acknowledged. The authors thank Rica Waterstadt for assistance in genotyping. This work was supported by grants from EU FP6 (EURO-RA), Hertie Stiftung, German Ministry of Education and Research (BMBF) through the National Genome Research Network (NGFN), Deutsche Forschungsgemeinschaft (KFO170) and the PopGen Biobank. The project received infrastructure support through the DFG excellence cluster {\textquoteleft}Inflammation at Interfaces{\textquoteright}. Benedicte A Lie and the Norwegian Bone Marrow Donor Registry at Rikshospita- let University Hospital, Oslo, are acknowledged for contributing the healthy Norwegian control population. Copyright: Copyright 2009 Elsevier B.V., All rights reserved.",

year = "2009",

doi = "10.1038/gene.2009.29",

language = "English",

volume = "10",

pages = "601--605",

journal = "Genes and Immunity",

issn = "1466-4879",

publisher = "Springer Nature",

number = "6",

}

TY - JOUR

T1 - Association of UCP2 -866 G/A polymorphism with chronic inflammatory diseases

AU - Yu, X.

AU - Wieczorek, S.

AU - Franke, A.

AU - Yin, H.

AU - Pierer, M.

AU - Sina, C.

AU - Karlsen, T. H.

AU - Boberg, K. M.

AU - Bergquist, A.

AU - Kunz, M.

AU - Witte, T.

AU - Gross, W. L.

AU - Epplen, J. T.

AU - Alarcón-Riquelme, M. E.

AU - Schreiber, S.

AU - Ibrahim, S. M.

N1 - Funding Information: The authors thank all patients, physicians and volunteer healthy controls for the cooperation. The cooperation of the Deutsche Morbus Crohn und Colitis Vereinigung e.V. and of the contributing gastroenterologists is gratefully acknowledged. The authors thank Rica Waterstadt for assistance in genotyping. This work was supported by grants from EU FP6 (EURO-RA), Hertie Stiftung, German Ministry of Education and Research (BMBF) through the National Genome Research Network (NGFN), Deutsche Forschungsgemeinschaft (KFO170) and the PopGen Biobank. The project received infrastructure support through the DFG excellence cluster ‘Inflammation at Interfaces’. Benedicte A Lie and the Norwegian Bone Marrow Donor Registry at Rikshospita- let University Hospital, Oslo, are acknowledged for contributing the healthy Norwegian control population. Copyright: Copyright 2009 Elsevier B.V., All rights reserved.

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

UR - https://www.scopus.com/pages/publications/69949186372

U2 - 10.1038/gene.2009.29

DO - 10.1038/gene.2009.29

M3 - Journal articles

C2 - 19387457

AN - SCOPUS:69949186372

SN - 1466-4879

VL - 10

SP - 601

EP - 605

JO - Genes and Immunity

JF - Genes and Immunity

IS - 6

ER -

Association of UCP2 -866 G/A polymorphism with chronic inflammatory diseases

Abstract

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