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Prostaglandins Other Lipid Mediat. 2015 Jul;120:103-14. doi: 10.1016/j.prostaglandins.2015.03.004. Epub 2015 Mar 26.

Dysregulation of gene expression in human fetal endothelial cells from gestational diabetes in response to TGF-β1.

Author information

1
Department of Neuroscience, Imaging and Clinical Sciences, G. d'Annunzio University, School of Medicine, and Center of Excellence on Aging (CeSI), Chieti, Italy.
2
School of Biomolecular & Biomedical Science Conway Institute, UCD, Dublin, Ireland.
3
Department of Drug Science, Padua University, Italy.
4
Institute of Obstetrics and Gynecology, Padua Hospital, Padua, Italy.
5
Department of Neuroscience, Imaging and Clinical Sciences, G. d'Annunzio University, School of Medicine, and Center of Excellence on Aging (CeSI), Chieti, Italy. Electronic address: ppatrignani@unich.it.

Abstract

Enhanced biosynthesis of several cytokines, such as, transforming growth factor-β1 (TGF-β1), is detected in gestational diabetes mellitus (GDM). In this study, we addressed the question of whether the exposure to the abnormal milieu of GDM in vivo affects gene expression pattern of human umbilical vein endothelial cells (HUVEC) in response to TGF-β1. We found that HUVEC isolated from GDM (dHUVEC) had reduced migratory capacity versus those of healthy women (nHUVEC) and this quiescent phenotype was associated with higher expression levels of the TGF-βtype I receptor ALK5 and a slight increase in the endogenous production of TGF-β1 (mainly in its latent form). Moreover, we performed transcriptome analysis, using microarray technology, of dHUVEC versus nHUVEC, after 3h treatment with exogenous TGF-β1 (10 ng/ml). The treatment of dHUVEC with TGF-β1 caused downregulation of the transcription of multiple genes involved in development, cell movement and migration of cells versus TGF-β1-treated nHUVEC. These changes in transcriptome profile might contribute to GDM-dependent alterations in cardiac morphogenesis and placental development.

KEYWORDS:

Gestational diabetes mellitus; HUVEC; Microarray; TGF-β

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