Abstract

Catechol-O-Methyltransferase (COMT) is a ubiquitous cytosolic enzyme expressed in many tissues responsible for the biotransformation of catechol compounds. 2-methoxyestradiol (2-ME2) is a metabolite of subsequent enzymatic o-methylation of 2-hydroxyestradiol via COMT. Its dose-dependent regulatory effects include inhibition of tubulin polymerization, migration, and proliferation in endothelial cells. Recent studies in engineered mice and human trophoblast cells suggest that perturbations in the COMT pathway along with subsequent decreased concentrations of 2-ME2 may be the link between preeclampsia and hypoxia.

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