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    A low COMT activity haplotype is associated with recurrent preeclampsia in a Norwegian population cohort (HUNT2)

    Access Status
    Open access via publisher
    Authors
    Roten, L.
    Fenstad, M.
    Forsmo, S.
    Johnson, M.
    Moses, Eric
    Austgulen, R.
    Skorpen, F.
    Date
    2011
    Type
    Journal Article
    
    Metadata
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    Citation
    Roten, L. and Fenstad, M. and Forsmo, S. and Johnson, M. and Moses, E. and Austgulen, R. and Skorpen, F. 2011. A low COMT activity haplotype is associated with recurrent preeclampsia in a Norwegian population cohort (HUNT2). Molecular Human Reproduction. 17 (7): pp. 439-446.
    Source Title
    Molecular Human Reproduction
    DOI
    10.1093/molehr/gar014
    ISSN
    1360-9947
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/17090
    Collection
    • Curtin Research Publications
    Abstract

    The etiology of preeclampsia is complex, with susceptibility being attributable to multiple environmental factors and a large genetic component. Although many candidate genes for preeclampsia have been suggested and studied, the specific causative genes still remain to be identified. Catechol-O-methyltransferase (COMT) is an enzyme involved in catecholamine and estrogen degradation and has recently been ascribed a role in development of preeclampsia. In the present study, we have examined the COMT gene by genotyping the functional Val108/158Met polymorphism (rs4680) and an additional single-nucleotide polymorphism, rs6269, predicting COMT activity haplotypes in a large Norwegian case/control cohort (ncases= 1135, ncontrols= 2262). A low COMT activity haplotype is associated with recurrent preeclampsia in our cohort. This may support the role of redox-regulated signaling and oxidative stress in preeclampsia pathogenesis as suggested by recent studies in a genetic mouse model. The COMT gene might be a genetic risk factor shared between preeclampsia and cardiovascular diseases.

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