MicroRNAs (miRNAs), small non-coding RNAs, have emerged as important, epigenetic regulators of endothelial function. Metabolic disturbances such as diabetes alter miRNA expression. In adults, the miRNA transcriptome as well as endothelial function differ between the sexes. Here, we hypothesized that metabolic disturbances associated with gestational diabetes (GDM) alter miRNA signatures in feto-placental endothelial cells (fpEC), dependent on fetal sex. We isolated human primary fpEC after normal and GDM-complicated pregnancies with male and female neonates and screened for differential miRNA expression using next-generation miRNA sequencing. To test for miRNAs commonly regulated in fpEC of female and male progeny, data were stratified for fetal sex and maternal body mass index (BMI). Analyses were also performed separately for female and male fpEC, again accounting for maternal BMI as covariate. Potential biological pathways regulated by the altered set of miRNAs were determined using mirPath software. Maternal GDM altered 26 miRNA signatures when male and female fpEC were analyzed together. Separate analysis of male versus female fpEC revealed 22 GDM affected miRNAs in the females and only 4 in the males, without overlap. Biological functions potentially modulated by the affected miRNAs related to ‘Protein Processing in Endoplasmic Reticulum’ and ‘Proteoglycans in Cancer’. Maternal GDM alters miRNA signatures in fpEC, and biological functions affected by these miRNAs relate to well-known adverse functional consequences of diabetes on endothelium. GDM effects were highly dependent on fetal sex with miRNA signatures in female fpEC being more susceptible to metabolic derangements of GDM than miRNAs in male fpEC.
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α-Smooth muscle actin staining of perinatal nicotine exposed bone marrow mesenchymal stem cells (BMSCs) upon myogenic induction. In Clinical Science volume 132, issue 21, Sakurai et al. report that perinatal nicotine-induced BMSC myofibroblast differentiation can be prevented by augmenting the lipofibroblast phenotype; for details, see pages 2357–2368.
Research Article|
November 22 2018
Gestational diabetes alters microRNA signatures in human feto-placental endothelial cells depending on fetal sex
Jasmin Strutz;
Jasmin Strutz
*
1Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria
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Silvija Cvitic;
Silvija Cvitic
*
1Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria
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Hubert Hackl;
Hubert Hackl
2Division of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
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Karl Kashofer;
Karl Kashofer
3Institute of Pathology, Medical University of Graz, Graz, Austria
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Hannah M. Appel;
Hannah M. Appel
1Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria
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Andrea Thüringer;
Andrea Thüringer
3Institute of Pathology, Medical University of Graz, Graz, Austria
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Gernot Desoye;
Gernot Desoye
1Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria
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Pieter Koolwijk;
Pieter Koolwijk
4Department of Physiology, VU University Medical Center, Amsterdam, The Netherlands
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Ursula Hiden
1Department of Obstetrics and Gynecology, Medical University of Graz, Graz, Austria
Correspondence: Ursula Hiden ([email protected])
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Publisher: Portland Press Ltd
Received:
September 18 2018
Revision Received:
October 24 2018
Accepted:
November 01 2018
Accepted Manuscript online:
November 02 2018
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2018
Clin Sci (Lond) (2018) 132 (22): 2437–2449.
Article history
Received:
September 18 2018
Revision Received:
October 24 2018
Accepted:
November 01 2018
Accepted Manuscript online:
November 02 2018
Connected Content
Citation
Jasmin Strutz, Silvija Cvitic, Hubert Hackl, Karl Kashofer, Hannah M. Appel, Andrea Thüringer, Gernot Desoye, Pieter Koolwijk, Ursula Hiden; Gestational diabetes alters microRNA signatures in human feto-placental endothelial cells depending on fetal sex. Clin Sci (Lond) 30 November 2018; 132 (22): 2437–2449. doi: https://doi.org/10.1042/CS20180825
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