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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...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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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 |
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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 |
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