The possible role of extravillous trophoblast-derived exosomes on the uterine spiral arterial remodeling under both normal and pathological conditions.

Carlos Salomon,Murray D Mitchell,Gregory E Rice,Sarah W Yee

doi:10.1155/2014/693157

Carlos Salomon, Murray D Mitchell + Show 2 more

Open Access

https://doi.org/10.1155/2014/693157

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Abstract

A tenet of contemporary obstetrics is that events that compromise placentation increase the risk of complications of pregnancy and contribute to poor pregnancy outcome. In particular, conditions that affect the invasion of placental cells and remodeling of uterine spiral arteries compromise placental function and the subsequent development of the fetus. Extravillous trophoblast cells (EVTs) proliferate and migrate from the cytotrophoblast in the anchoring villi of the placenta and invade the maternal decidua and myometrium. These cells are localised with uterine uterine spiral arteries and are thought to induce vascular remodeling. A newly identified pathway by which EVTs may regulate vascular remodeling within the uterus is via the release of exosomes. Trophoblast cells release exosomes that mediate aspects of cell-to-cell communication. The aim of this brief commentary is to review the putative role of exosomes released from extravillous trophoblast cells in uterine spiral artery remodeling and, in particular, their role in the aetiology of preeclampsia. Placental exosomes may engage in local cell-to-cell communication between the cell constituents of the placenta and contiguous maternal tissues and/or distal interactions, involving the release of placental exosomes into biological fluids and their transport to a remote site of action.

Highlights

A successful outcome to pregnancy is critically dependent upon events that affect implantation and early development of the placenta [1]
Exosomes are sensitive to environmental milieu, changing their bioactivity and content; we propose that, under physiological conditions, placental exosomes promote vascular cell migration from the uterine spiral arteries; under pathological conditions, the bioactivity of placental exosomes is reduced
Extravillous trophoblast cells (EVTs) migrate into maternal decidua and myometrium and interact with endothelial and vascular smooth muscle cells in uterine spiral arteries

Summary

Introduction

A successful outcome to pregnancy is critically dependent upon events that affect implantation and early development of the placenta [1]. While the mechanisms by which EVTs remodel SpA remain to be fully elucidated, available data are consistent with the hypothesis that EVTs directly interact with vascular smooth muscle cells of uterine spiral arteries and affect their loss. We know little about the mechanism by which exosomal packaging occurs, they contain a diverse array of signalling molecules and are released from the parent cell following the exocytotic fusion of multivesicular bodies with the cell membrane [12]. In this brief commentary, we develop the working hypothesis that exosomal signalling plays a critical role in normal. BioMed Research International placentation and that disruption of exosomal pathways (and in particular the release of exosomes from EVTs) plays a key role in the pathogenesis of complications of pregnancy, including preeclampsia

EVTs and Uterine Spiral Artery Remodeling

Microenvironmental Factors

Exosomes

Findings

Summary