Severe Early-Onset Preeclampsia Is Not Associated with a Change in Placental Catechol O-Methyltransferase (COMT) Expression

Kirsten Palmer, Burcu Saglam, Clare Whitehead, Owen Stock, Martha Lappas, Steven Tong

    Research output: Contribution to journalArticle

    18 Citations (Scopus)

    Abstract

    The genetic deletion of catechol O-methyltransferase (COMT) in mice produces a preeclampsia-like phenotype, with mice exhibiting hypertension, proteinuria, and histological changes, consistent with human pathological features. 2-Methoxyoestradiol, a metabolite of COMT, increases human trophoblast invasiveness in vitro under hypoxic conditions, providing further support that decreased COMT expression may have a role in preeclampsia. However, evidence confirming decreased COMT expression in human disease has been limited to small studies of placentas obtained from cases of term preeclampsia. We examined COMT expression in placentas obtained from healthy term pregnancies (n = 14), preterm normotensive pregnancies (n = 8), and pregnancies complicated by severe preterm preeclampsia (delivery at<34 weeks' gestation; n = 22). Among our preeclamptic cohort were 10 pregnancies further complicated by HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets); and one pregnancy complicated by an eclamptic seizure. COMT expression was analyzed by RT-PCR, Western analysis, and IHC. COMT was mainly expressed in the syncytiotrophoblast. We did not find a significant difference in placental COMT expression in severe preeclampsia compared with either term or preterm normotensive cohorts. Our results suggest that severe preeclampsia may not be associated with a decrease in placental COMT expression.

    Original languageEnglish
    Pages (from-to)2484-2488
    Number of pages5
    JournalAmerican Journal of Pathology
    Volume178
    Issue number6
    DOIs
    Publication statusPublished - 2011

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