Cargando…

Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling

Vascular tubulogenesis is tightly linked with physiological and pathological events in the living body. Endothelial cells (ECs), which are constantly exposed to hemodynamic forces, play a key role in tubulogenesis. Hydrostatic pressure in particular has been shown to elicit biophysical and biochemic...

Descripción completa

Detalles Bibliográficos
Autores principales: Yoshino, Daisuke, Funamoto, Kenichi, Sato, Kakeru, Kenry, Sato, Masaaki, Lim, Chwee Teck
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118103/
https://www.ncbi.nlm.nih.gov/pubmed/32242084
http://dx.doi.org/10.1038/s42003-020-0881-9
_version_ 1783514490091864064
author Yoshino, Daisuke
Funamoto, Kenichi
Sato, Kakeru
Kenry
Sato, Masaaki
Lim, Chwee Teck
author_facet Yoshino, Daisuke
Funamoto, Kenichi
Sato, Kakeru
Kenry
Sato, Masaaki
Lim, Chwee Teck
author_sort Yoshino, Daisuke
collection PubMed
description Vascular tubulogenesis is tightly linked with physiological and pathological events in the living body. Endothelial cells (ECs), which are constantly exposed to hemodynamic forces, play a key role in tubulogenesis. Hydrostatic pressure in particular has been shown to elicit biophysical and biochemical responses leading to EC-mediated tubulogenesis. However, the relationship between tubulogenesis and hydrostatic pressure remains to be elucidated. Here, we propose a specific mechanism through which hydrostatic pressure promotes tubulogenesis. We show that pressure exposure transiently activates the Ras/extracellular signal-regulated kinase (ERK) pathway in ECs, inducing endothelial tubulogenic responses. Water efflux through aquaporin 1 and activation of protein kinase C via specific G protein–coupled receptors are essential to the pressure-induced transient activation of the Ras/ERK pathway. Our approach could provide a basis for elucidating the mechanopathology of tubulogenesis-related diseases and the development of mechanotherapies for improving human health.
format Online
Article
Text
id pubmed-7118103
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher Nature Publishing Group UK
record_format MEDLINE/PubMed
spelling pubmed-71181032020-04-06 Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling Yoshino, Daisuke Funamoto, Kenichi Sato, Kakeru Kenry Sato, Masaaki Lim, Chwee Teck Commun Biol Article Vascular tubulogenesis is tightly linked with physiological and pathological events in the living body. Endothelial cells (ECs), which are constantly exposed to hemodynamic forces, play a key role in tubulogenesis. Hydrostatic pressure in particular has been shown to elicit biophysical and biochemical responses leading to EC-mediated tubulogenesis. However, the relationship between tubulogenesis and hydrostatic pressure remains to be elucidated. Here, we propose a specific mechanism through which hydrostatic pressure promotes tubulogenesis. We show that pressure exposure transiently activates the Ras/extracellular signal-regulated kinase (ERK) pathway in ECs, inducing endothelial tubulogenic responses. Water efflux through aquaporin 1 and activation of protein kinase C via specific G protein–coupled receptors are essential to the pressure-induced transient activation of the Ras/ERK pathway. Our approach could provide a basis for elucidating the mechanopathology of tubulogenesis-related diseases and the development of mechanotherapies for improving human health. Nature Publishing Group UK 2020-04-02 /pmc/articles/PMC7118103/ /pubmed/32242084 http://dx.doi.org/10.1038/s42003-020-0881-9 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Yoshino, Daisuke
Funamoto, Kenichi
Sato, Kakeru
Kenry
Sato, Masaaki
Lim, Chwee Teck
Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
title Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
title_full Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
title_fullStr Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
title_full_unstemmed Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
title_short Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
title_sort hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and ras-erk signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118103/
https://www.ncbi.nlm.nih.gov/pubmed/32242084
http://dx.doi.org/10.1038/s42003-020-0881-9
work_keys_str_mv AT yoshinodaisuke hydrostaticpressurepromotesendothelialtubeformationthroughaquaporin1andraserksignaling
AT funamotokenichi hydrostaticpressurepromotesendothelialtubeformationthroughaquaporin1andraserksignaling
AT satokakeru hydrostaticpressurepromotesendothelialtubeformationthroughaquaporin1andraserksignaling
AT kenry hydrostaticpressurepromotesendothelialtubeformationthroughaquaporin1andraserksignaling
AT satomasaaki hydrostaticpressurepromotesendothelialtubeformationthroughaquaporin1andraserksignaling
AT limchweeteck hydrostaticpressurepromotesendothelialtubeformationthroughaquaporin1andraserksignaling