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Fetoplacental endothelial exosomes modulate high d-glucose-induced endothelial dysfunction

Tamara Sáez¹, Paul de Vos², Jeroen Kuipers³

¹Immunoendocrinology, Division of Medical Biology, Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands; Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, 8330024, Chile.

|June 10, 2018

Summary

High glucose levels in gestational diabetes mellitus induce endothelial dysfunction. Endothelial exosomes from high glucose conditions mimic these effects, impacting fetoplacental vasculature.

Area of Science:

Endocrinology and Metabolism
Vascular Biology
Cellular and Molecular Medicine

Background:

Gestational diabetes mellitus (GDM) is linked to fetoplacental endothelial dysfunction, potentially caused by hyperglycemia.
Endothelial exosomes, nanovesicles influencing endothelial function, are investigated for their role in high glucose-induced dysfunction.

Purpose of the Study:

To investigate the role of endothelial exosomes in high glucose-induced endothelial dysfunction in the context of GDM.
To determine if exosomes derived from high glucose-exposed endothelial cells replicate the effects of hyperglycemia on endothelial function.

Main Methods:

Isolated exosomes from human umbilical vein endothelial cells (HUVECs) cultured in basal glucose (exo-BG) and high glucose (exo-HG) conditions.
Characterized exosomes using ultracentrifugation, electron microscopy, and nanotracking analysis.
Assessed the impact of exosomes on HUVEC function, including wound healing, and expression of key proteins (e.g., eNOS, hCAT-1, VEGF, ICAM-1).

Main Results:

High glucose increased exosome release from HUVECs and enhanced endothelial wound healing and expression of phosphorylated eNOS, hCAT-1, VEGF, and ICAM-1.
Exosomes from high glucose conditions (exo-HG) promoted endothelial wound healing and increased specific protein expressions in normoglycemic HUVECs.
Exosomes from basal glucose conditions (exo-BG) partially reversed the effects of high glucose on endothelial wound healing and hCAT-1 expression.

Conclusions:

High glucose can induce endothelial dysfunction in HUVECs, and exosomes from these cells mimic some of these detrimental effects.
This study elucidates a potential mechanism by which hyperglycemia contributes to fetoplacental vascular issues in GDM.
Endothelial exosomes represent a significant factor in the pathogenesis of GDM-associated endothelial dysfunction.

Keywords:

Endothelial dysfunction Exosomes Fetoplacental vasculature Gestational diabetes High glucose

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