Association of a common polymorphism in the promoter of UCP2 with susceptibility to multiple sclerosis

Susanne Vogler; René Goedde; Bianca Miterski; Ralf Gold; Antje Kroner; Dirk Koczan; Uwe Klaus Zettl; Peter Rieckmann; Joerg T. Epplen; Saleh M. Ibrahim

doi:10.1007/s00109-005-0661-5

Association of a common polymorphism in the promoter of UCP2 with susceptibility to multiple sclerosis

Susanne Vogler, René Goedde, Bianca Miterski, Ralf Gold, Antje Kroner, Dirk Koczan, Uwe Klaus Zettl, Peter Rieckmann, Joerg T. Epplen, Saleh M. Ibrahim^*

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

Klinik für Dermatologie, Allergologie und Venerologie

62 Zitate (Scopus)

Abstract

Uncoupling protein 2 (UCP2) is a member of the mitochondrial proton transport family that uncouples proton entry to the mitochondria from ATP synthesis. UCP2 expression levels have been linked to predisposition to diabetes and obesity. In addition, UCP2 prevents neuronal death and injury. Here we show that the common -866G/A promoter polymorphism is associated with susceptibility to multiple sclerosis (MS) in the German population. We analysed altogether 1,097 MS patients and 462 control subjects from two cohorts and found that the common G allele is associated with disease susceptibility (p=0.0015). The UCP2 -866G allele is correlated with lower levels of UCP2 expression as shown here in vitro and in vivo. Thus, UCP2 promoter polymorphism may contribute to MS susceptibility by regulating the level of UCP2 protein in the central nervous and/or the immune systems.

Originalsprache	Englisch
Zeitschrift	Journal of Molecular Medicine
Jahrgang	83
Ausgabenummer	10
Seiten (von - bis)	806-811
Seitenumfang	6
ISSN	0946-2716
DOIs	https://doi.org/10.1007/s00109-005-0661-5
Publikationsstatus	Veröffentlicht - 10.2005

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Acknowledgements We would like to thank Rica Waterstradt, Ildikó Tóth and Andrea Petzold for excellent technical assistance. This study was funded in part by the German Federal Ministry of Research and Education (FKZ 01ZZ0108) and by Hertie Stiftung (1.319.110/02/05).

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10.1007/s00109-005-0661-5

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title = "Association of a common polymorphism in the promoter of UCP2 with susceptibility to multiple sclerosis",

abstract = "Uncoupling protein 2 (UCP2) is a member of the mitochondrial proton transport family that uncouples proton entry to the mitochondria from ATP synthesis. UCP2 expression levels have been linked to predisposition to diabetes and obesity. In addition, UCP2 prevents neuronal death and injury. Here we show that the common -866G/A promoter polymorphism is associated with susceptibility to multiple sclerosis (MS) in the German population. We analysed altogether 1,097 MS patients and 462 control subjects from two cohorts and found that the common G allele is associated with disease susceptibility (p=0.0015). The UCP2 -866G allele is correlated with lower levels of UCP2 expression as shown here in vitro and in vivo. Thus, UCP2 promoter polymorphism may contribute to MS susceptibility by regulating the level of UCP2 protein in the central nervous and/or the immune systems.",

author = "Susanne Vogler and Ren{\'e} Goedde and Bianca Miterski and Ralf Gold and Antje Kroner and Dirk Koczan and Zettl, \{Uwe Klaus\} and Peter Rieckmann and Epplen, \{Joerg T.\} and Ibrahim, \{Saleh M.\}",

note = "Funding Information: Acknowledgements We would like to thank Rica Waterstradt, Ildik{\'o} T{\'o}th and Andrea Petzold for excellent technical assistance. This study was funded in part by the German Federal Ministry of Research and Education (FKZ 01ZZ0108) and by Hertie Stiftung (1.319.110/02/05).",

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doi = "10.1007/s00109-005-0661-5",

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T1 - Association of a common polymorphism in the promoter of UCP2 with susceptibility to multiple sclerosis

AU - Vogler, Susanne

AU - Goedde, René

AU - Miterski, Bianca

AU - Gold, Ralf

AU - Kroner, Antje

AU - Koczan, Dirk

AU - Zettl, Uwe Klaus

AU - Rieckmann, Peter

AU - Epplen, Joerg T.

AU - Ibrahim, Saleh M.

N1 - Funding Information: Acknowledgements We would like to thank Rica Waterstradt, Ildikó Tóth and Andrea Petzold for excellent technical assistance. This study was funded in part by the German Federal Ministry of Research and Education (FKZ 01ZZ0108) and by Hertie Stiftung (1.319.110/02/05).

PY - 2005/10

Y1 - 2005/10

N2 - Uncoupling protein 2 (UCP2) is a member of the mitochondrial proton transport family that uncouples proton entry to the mitochondria from ATP synthesis. UCP2 expression levels have been linked to predisposition to diabetes and obesity. In addition, UCP2 prevents neuronal death and injury. Here we show that the common -866G/A promoter polymorphism is associated with susceptibility to multiple sclerosis (MS) in the German population. We analysed altogether 1,097 MS patients and 462 control subjects from two cohorts and found that the common G allele is associated with disease susceptibility (p=0.0015). The UCP2 -866G allele is correlated with lower levels of UCP2 expression as shown here in vitro and in vivo. Thus, UCP2 promoter polymorphism may contribute to MS susceptibility by regulating the level of UCP2 protein in the central nervous and/or the immune systems.

AB - Uncoupling protein 2 (UCP2) is a member of the mitochondrial proton transport family that uncouples proton entry to the mitochondria from ATP synthesis. UCP2 expression levels have been linked to predisposition to diabetes and obesity. In addition, UCP2 prevents neuronal death and injury. Here we show that the common -866G/A promoter polymorphism is associated with susceptibility to multiple sclerosis (MS) in the German population. We analysed altogether 1,097 MS patients and 462 control subjects from two cohorts and found that the common G allele is associated with disease susceptibility (p=0.0015). The UCP2 -866G allele is correlated with lower levels of UCP2 expression as shown here in vitro and in vivo. Thus, UCP2 promoter polymorphism may contribute to MS susceptibility by regulating the level of UCP2 protein in the central nervous and/or the immune systems.

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Association of a common polymorphism in the promoter of UCP2 with susceptibility to multiple sclerosis

Abstract

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