Emerging concepts of shear stress in placental development and function.
Piezo1
endothelial cells
mechanosensing
placenta
shear stress
Journal
Molecular human reproduction
ISSN: 1460-2407
Titre abrégé: Mol Hum Reprod
Pays: England
ID NLM: 9513710
Informations de publication
Date de publication:
06 06 2019
06 06 2019
Historique:
received:
15
10
2018
revised:
03
03
2019
pubmed:
2
4
2019
medline:
19
5
2020
entrez:
2
4
2019
Statut:
ppublish
Résumé
Blood flow, and the force it generates, is critical to placental development and function throughout pregnancy. This mechanical stimulation of cells by the friction generated from flow is called shear stress (SS) and is a fundamental determinant of vascular homeostasis, regulating remodelling and vasomotor tone. This review describes how SS is fundamental to the establishment and regulation of the blood flow through the uteroplacental and fetoplacental circulations. Amongst the most recent findings is that alongside the endothelium, embryonic stem cells and the villous trophoblast are mechanically sensitive. A complex balance of forces is required to enable effective establishment of the uteroplacental circulation, while protecting the embryo and placental villi. SS also generates flow-mediated vasodilatation through the release of endothelial nitric oxide, a process vital for adequate placental blood flow. The identification of SS sensors and the mechanisms governing how the force is converted into biochemical signals is a fast-paced area of research, with multiple cellular components under investigation. For example, the Piezo1 ion channel is mechanosensitive in a variety of tissues including the fetoplacental endothelium. Enhanced Piezo1 activity has been demonstrated in response to the Yoda1 agonist molecule, suggesting the possibility for developing tools to manipulate these channels. Whether such agents might progress to novel therapeutics to improve blood flow through the placenta requires further consideration and research.
Identifiants
pubmed: 30931481
pii: 5424050
doi: 10.1093/molehr/gaz018
pmc: PMC6554190
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
329-339Subventions
Organisme : Medical Research Council
ID : MR/P002099/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/17/11/33042
Pays : United Kingdom
Informations de copyright
© The Author(s) 2019. Published by Oxford University Press.
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