Association of deficiencies of catechol-O-methyltransferase and 2-methoxyestradiol with preeclampsia

Katherine W. Arendt, Vesna D. Garovic

Research output: Contribution to journalComment/debatepeer-review

2 Scopus citations

Abstract

Evaluation of: Kanasaki K, Palmsten K, Sugimoto H et al. Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia. Nature 453 (7198), 1117-1121 (2008). Despite recent advances in the understanding of dysregulation of placenta-derived anti-angiogenic factors in preeclampsia, the etiology and pathogenesis of this disorder remain elusive. Catechol-O-methyltransferase (COMT) generates 2-methoxyestradiol (2-ME) in the human placenta and has been shown to have decreased activity in the placenta in severe preeclampsia. Kanasaki and colleagues performed a series of experiments in a Comt -/- mouse model, showing that decreased COMT activity and subsequent decreased 2-ME levels resulted in the clinical, histologic and molecular changes characteristic of preeclampsia. Furthermore, both the preeclampsia-like clinical features and characteristic angiogenic abnormalities completely resolved in rescue experiments with 2-ME. In addition, circulating levels of 2-ME were lower in eight women with preeclampsia compared with 13 normotensive pregnant controls. These preliminary data suggest that 2-ME may serve both as a marker and as a therapeutic target in preeclampsia; thus, setting the stage for future comprehensive validation studies in larger patient cohorts.

Original languageEnglish (US)
Pages (from-to)379-381
Number of pages3
JournalExpert Review of Obstetrics and Gynecology
Volume4
Issue number4
DOIs
StatePublished - Jul 1 2009

Keywords

  • 2-methoxyestradiol
  • Angiogenesis
  • Catechol-O-methyltransferase
  • Endothelial dysfunction
  • Preeclampsia
  • VEGF
  • VEGF receptor

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Reproductive Medicine
  • Obstetrics and Gynecology
  • Maternity and Midwifery

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