Floris, Ilaria and Descamps, Betty and Vardeu, Antonella and Mitić, Tijana and Posadino, Anna Maria and Shantikumar, Saran and Sala-Newby, Graciela and Capobianco, Giampiero and Mangialardi, Giuseppe and Howard, Lynsey and Dessole, Salvatore and Urrutia, Raul and Pintus, Gianfranco and Emanueli, Costanza (2015) Gestational diabetes mellitus impairs fetal endothelial cell functions through a mechanism involving microRNA-101 and histone methyltransferase enhancer of zester homolog-2 (Translational Sciences). Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 35 , p. 664-674. eISSN 1524-4636. Article.
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Objective: Gestational diabetes mellitus (GDM) produces fetal hyperglycemia with increased lifelong risks for the exposed offspring of cardiovascular and other diseases. Epigenetic mechanisms induce long-term gene expression changes in response to in utero environmental perturbations. Moreover, microRNAs (miRs) control the function of endothelial cells (ECs) under physiological and pathological conditions and can target the epigenetic machinery. We investigated the functional and expressional effect of GDM on human fetal ECs of the umbilical cord vein (HUVECs). We focused on miR-101 and 1 of its targets, enhancer of zester homolog-2 (EZH2), which trimethylates the lysine 27 of histone 3, thus repressing gene transcription. EZH2 exists as isoforms α and β.
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