Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters










Database
Language
Publication year range
1.
Biomed Res Int ; 2014: 693157, 2014.
Article in English | MEDLINE | ID: mdl-25302305

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.


Subject(s)
Chorionic Villi/physiopathology , Exosomes/physiology , Models, Cardiovascular , Pre-Eclampsia/physiopathology , Trophoblasts/physiology , Uterine Artery/physiopathology , Chorionic Villi/pathology , Exosomes/pathology , Female , Humans , Pre-Eclampsia/pathology , Pregnancy , Trophoblasts/pathology , Uterine Artery/pathology
SELECTION OF CITATIONS
SEARCH DETAIL
...