Purpose: Deficiencies in placental catechol-O-methyltransferase (COMT) and circulating 2-methoxyoestradiol (2-ME) have been shown to be related to early onset preeclampsia. The aim of this study was to investigate levels of 2-ME in the serum and urine of patients with late-onset preeclampsia and to compare those levels to those of normal pregnant women. In addition, we examined placental COMT expression in both groups.
Methods: Fifteen patients with preeclampsia and 15 normal pregnant women were enrolled. 2-ME levels were evaluated by ELISA and placental COMT expression was examined by Western blot analysis.
Results: 2-ME levels in serum [median 181.1 pg/mL, interquartile range (IQR) 119.6-244.3 vs. 61.2 pg/mL, IQR 12.0-133.7, respectively, p = 0.004] and urine (median 143.3 pg/mL, IQR 35.0-328.2 vs. 0.5 pg/mL, IQR 0.4-4.6, respectively, p < 0.001) were significantly increased in patients with late-onset preeclampsia compared to those in normal pregnant women at term. There was no significant difference in placental COMT expression between the two groups.
Conclusion: Increased levels of 2-ME in patients with late-onset preeclampsia might be a product of a compensatory mechanism in patients with late-onset preeclampsia.
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http://dx.doi.org/10.1007/s00404-012-2663-1 | DOI Listing |
Mol Med Rep
April 2021
Department of Biomaterials Science (BK21 FOUR Program), College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Miryang, Gyeongsangnam 50463, Republic of Korea.
Reprod Sci
February 2021
Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas, USA.
Catechol-O-methyltransferase (COMT) has been shown to be a key regulator of pregnancy outcomes in mouse, and its deficiency is causative in the development of a preeclampsia-like disease process. Preeclampsia is a human pregnancy disorder associated with failure of intrauterine trophoblast cell invasion and trophoblast-guided uterine spiral artery remodeling, which are not well-developed in mouse. The purpose of this study was to investigate COMT in rat, a species with deep intrauterine trophoblast invasion.
View Article and Find Full Text PDFReprod Toxicol
June 2019
Department of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Jagiellonian University in Kraków, Kraków, Poland. Electronic address:
We determined the action of a mixture of 16 priority PAHs present in high concentrations in maternal blood (Mix I) and the same but in low concentrations detected in placental tissue (Mix II) on AhR, ERα, NFκB, CYP1A1, CYP1B1, and COMT protein expression and cell proliferation of JEG-3 and BeWo cell lines. Both mixtures induced AhR expression in JEG-3 and BeWo; however, in JEG-3 cells expression of ERα, CYP1A1, CYP1B1, and COMT was upregulated, while in BeWo cells downregulated. The opposite effect of mixtures on NFκB protein expression (inhibitory in JEG-3, stimulatory in BeWo) was noted.
View Article and Find Full Text PDFInt J Obes (Lond)
November 2019
Department of Physiology and Pharmacology, Karolinska Institutet, Solna, Sweden.
Background/objectives: Maternal obesity together with androgen excess in mice negatively affects placental function and maternal and fetal liver function as demonstrated by increased triglyceride content with dysfunctional expression of enzymes and transcription factors involved in de novo lipogenesis and fat storage. To identify changes in molecular pathways that might promote diseases in adulthood, we performed a global proteomic analysis using a liquid-chromatography/mass-spectrometry system to investigate total and phosphorylated proteins in the placenta and fetal liver in a mouse model that combines maternal obesity with maternal androgen excess.
Methods: After ten weeks on a control diet (CD) or high fat/high sugar-diet, dams were mated with males fed the CD.
Int J Mol Sci
October 2018
Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Although the global maternal mortality ratio has been consistently reduced over time, in 2015, there were still 303,000 maternal deaths throughout the world, of which 99% occurred in developing countries. Understanding pathophysiology of pregnancy complications contributes to the proper prenatal care for the reduction of prenatal, perinatal and neonatal mortality and morbidity ratio. In this review, we focus on AMP-activated protein kinase (AMPK) as a regulator of pregnancy complications.
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