Cited by 381Pregnancy and preeclampsia studiesNeurological Complications and SyndromesEicosanoids and Hypertension Pharmacology

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Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia

Kanasaki, Keizo, Palmsten, Kristin, Sugimoto, Hikaru, Ahmad, Shakil, Hamano, Yuki, Xie, Liang, Parry, Samuel, Augustin, Hellmut G., Gattone, Vincent H., Folkman, Judah, Strauss, Jerome F., Kalluri, Raghu·2008·Nature

DOI 10.1038/nature06951

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Abstract

Despite intense investigation, mechanisms that facilitate the emergence of the pre-eclampsia phenotype in women are still unknown. Placental hypoxia, hypertension, proteinuria and oedema are the principal clinical features of this disease. It is speculated that hypoxia-driven disruption of the angiogenic balance involving vascular endothelial growth factor (VEGF)/placenta-derived growth factor (PLGF) and soluble Fms-like tyrosine kinase-1 (sFLT-1, the soluble form of VEGF receptor 1) might contribute to some of the maternal symptoms of pre-eclampsia. However, pre-eclampsia does not develop in all women with high sFLT-1 or low PLGF levels, and it also occurs in some women with low sFLT-1 and high PLGF levels. Moreover, recent experiments strongly suggest that several soluble factors affecting the vasculature are probably elevated because of placental hypoxia in the pre-eclamptic women, indicating that upstream molecular defect(s) may contribute to pre-eclampsia. Here we show that pregnant mice deficient in catechol-O-methyltransferase (COMT) show a pre-eclampsia-like phenotype resulting from an absence of 2-methoxyoestradiol (2-ME), a natural metabolite of oestradiol that is elevated during the third trimester of normal human pregnancy. 2-ME ameliorates all pre-eclampsia-like features without toxicity in the Comt(-/-) pregnant mice and suppresses placental hypoxia, hypoxia-inducible factor-1alpha expression and sFLT-1 elevation. The levels of COMT and 2-ME are significantly lower in women with severe pre-eclampsia. Our studies identify a genetic mouse model for pre-eclampsia and suggest that 2-ME may have utility as a plasma and urine diagnostic marker for this disease, and may also serve as a therapeutic supplement to prevent or treat this disorder.

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Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
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Authors: Kanasaki, K., Palmsten, K., Sugimoto, H., Ahmad, S., Hamano, Y., Xie, L., Parry, S., Augustin, H. G., Gattone, V. H., Folkman, J., Strauss, J. F., & Kalluri, R.
Affiliations: Beth Israel Deaconess Medical Center (US)
Birmingham Women's Hospital (GB)
University of Pennsylvania (US)
German Cancer Research Center (DE)
Indiana University Indianapolis (US)
Boston Children's Hospital (US)
Virginia Commonwealth University (US)
Corresponding author: Kalluri, Raghu
ORCID: Kanasaki, Keizo
Palmsten, Kristin
Sugimoto, Hikaru
Ahmad, Shakil
Xie, Liang
Parry, Samuel
Augustin, Hellmut G.
Strauss, Jerome F.
Kalluri, Raghu
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2008-05-11
Volume: 453
Issue: 7198
Pages: 1117-1121
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature06951
OpenAlex: W2066278927
Cited by: 381
References: 34
Citations by year: 2026: 4 · 2025: 12 · 2024: 8 · 2023: 8 · 2022: 13 · 2021: 18 · 2020: 22 · 2019: 27 · 2018: 28 · 2017: 31 · 2016: 16 · 2015: 22 · 2014: 29 · 2013: 22 · 2012: 29
FWCI: 34.71
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
RePEc: Research Papers in Economics (submittedVersion)
University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
Funders: Beth Israel Deaconess Medical Center
University of Pennsylvania
British Heart Foundation
Fondation pour la Recherche Médicale
Georg-August-Universität Göttingen
Kanae Foundation for the Promotion of Medical Science
National Institutes of Health
Medical Research Council
National Institute of Diabetes and Digestive and Kidney Diseases (DK 62987, DK61688, R01DK062987, DK 13193, DK-55001, R01DK061688, R01DK055001)
Topics: Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Health Sciences › Medicine › Clinical Neurology › Neurological Complications and Syndromes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords: preeclampsia, catechol-O-methyltransferase, 2-methoxyestradiol, placental hypoxia, angiogenic imbalance, soluble fms-like tyrosine kinase-1, vascular endothelial growth factor, placental growth factor, placenta, pregnancy complications, therapeutic target, proteinuria, hypertension, edema
MeSH terms: 2-Methoxyestradiol, Albumins, Animals, Hypoxia, Blood Pressure, Catechol O-Methyltransferase, Creatinine, Disease Models, Animal, Estradiol, Female, Humans, Hypertension, Killer Cells, Natural, Litter Size, Male, Placenta, Pre-Eclampsia, Pregnancy, Proteinuria, Vascular Endothelial Growth Factor Receptor-1, Mice, Hypoxia-Inducible Factor 1, alpha Subunit

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Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia

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