Cargando…

High intraluminal pressure promotes vascular inflammation via caveolin-1

The aetiology and progression of hypertension involves various endogenous systems, such as the renin angiotensin system, the sympathetic nervous system, and endothelial dysfunction. Recent data suggest that vascular inflammation may also play a key role in the pathogenesis of hypertension. This stud...

Descripción completa

Detalles Bibliográficos
Autores principales: Michell, Danielle L., Shihata, Waled A., Andrews, Karen L., Abidin, Nurul Aisha Zainal, Jefferis, Ann-Maree, Sampson, Amanda K., Lumsden, Natalie G., Huet, Olivier, Parat, Marie-Odile, Jennings, Garry L., Parton, Robert G., Woollard, Kevin J., Kaye, David M., Chin-Dusting, Jaye P. F., Murphy, Andrew J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7960707/
https://www.ncbi.nlm.nih.gov/pubmed/33723357
http://dx.doi.org/10.1038/s41598-021-85476-z
_version_ 1783665109943451648
author Michell, Danielle L.
Shihata, Waled A.
Andrews, Karen L.
Abidin, Nurul Aisha Zainal
Jefferis, Ann-Maree
Sampson, Amanda K.
Lumsden, Natalie G.
Huet, Olivier
Parat, Marie-Odile
Jennings, Garry L.
Parton, Robert G.
Woollard, Kevin J.
Kaye, David M.
Chin-Dusting, Jaye P. F.
Murphy, Andrew J.
author_facet Michell, Danielle L.
Shihata, Waled A.
Andrews, Karen L.
Abidin, Nurul Aisha Zainal
Jefferis, Ann-Maree
Sampson, Amanda K.
Lumsden, Natalie G.
Huet, Olivier
Parat, Marie-Odile
Jennings, Garry L.
Parton, Robert G.
Woollard, Kevin J.
Kaye, David M.
Chin-Dusting, Jaye P. F.
Murphy, Andrew J.
author_sort Michell, Danielle L.
collection PubMed
description The aetiology and progression of hypertension involves various endogenous systems, such as the renin angiotensin system, the sympathetic nervous system, and endothelial dysfunction. Recent data suggest that vascular inflammation may also play a key role in the pathogenesis of hypertension. This study sought to determine whether high intraluminal pressure results in vascular inflammation. Leukocyte adhesion was assessed in rat carotid arteries exposed to 1 h of high intraluminal pressure. The effect of intraluminal pressure on signaling mechanisms including reactive oxygen species production (ROS), arginase expression, and NFĸB translocation was monitored. 1 h exposure to high intraluminal pressure (120 mmHg) resulted in increased leukocyte adhesion and inflammatory gene expression in rat carotid arteries. High intraluminal pressure also resulted in a downstream signaling cascade of ROS production, arginase expression, and NFĸB translocation. This process was found to be angiotensin II-independent and mediated by the mechanosensor caveolae, as caveolin-1 (Cav1)-deficient endothelial cells and mice were protected from pressure-induced vascular inflammatory signaling and leukocyte adhesion. Cav1 deficiency also resulted in a reduction in pressure-induced glomerular macrophage infiltration in vivo. These findings demonstrate Cav1 is an important mechanosensor in pressure-induced vascular and renal inflammation.
format Online
Article
Text
id pubmed-7960707
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Nature Publishing Group UK
record_format MEDLINE/PubMed
spelling pubmed-79607072021-03-19 High intraluminal pressure promotes vascular inflammation via caveolin-1 Michell, Danielle L. Shihata, Waled A. Andrews, Karen L. Abidin, Nurul Aisha Zainal Jefferis, Ann-Maree Sampson, Amanda K. Lumsden, Natalie G. Huet, Olivier Parat, Marie-Odile Jennings, Garry L. Parton, Robert G. Woollard, Kevin J. Kaye, David M. Chin-Dusting, Jaye P. F. Murphy, Andrew J. Sci Rep Article The aetiology and progression of hypertension involves various endogenous systems, such as the renin angiotensin system, the sympathetic nervous system, and endothelial dysfunction. Recent data suggest that vascular inflammation may also play a key role in the pathogenesis of hypertension. This study sought to determine whether high intraluminal pressure results in vascular inflammation. Leukocyte adhesion was assessed in rat carotid arteries exposed to 1 h of high intraluminal pressure. The effect of intraluminal pressure on signaling mechanisms including reactive oxygen species production (ROS), arginase expression, and NFĸB translocation was monitored. 1 h exposure to high intraluminal pressure (120 mmHg) resulted in increased leukocyte adhesion and inflammatory gene expression in rat carotid arteries. High intraluminal pressure also resulted in a downstream signaling cascade of ROS production, arginase expression, and NFĸB translocation. This process was found to be angiotensin II-independent and mediated by the mechanosensor caveolae, as caveolin-1 (Cav1)-deficient endothelial cells and mice were protected from pressure-induced vascular inflammatory signaling and leukocyte adhesion. Cav1 deficiency also resulted in a reduction in pressure-induced glomerular macrophage infiltration in vivo. These findings demonstrate Cav1 is an important mechanosensor in pressure-induced vascular and renal inflammation. Nature Publishing Group UK 2021-03-15 /pmc/articles/PMC7960707/ /pubmed/33723357 http://dx.doi.org/10.1038/s41598-021-85476-z Text en © The Author(s) 2021 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Michell, Danielle L.
Shihata, Waled A.
Andrews, Karen L.
Abidin, Nurul Aisha Zainal
Jefferis, Ann-Maree
Sampson, Amanda K.
Lumsden, Natalie G.
Huet, Olivier
Parat, Marie-Odile
Jennings, Garry L.
Parton, Robert G.
Woollard, Kevin J.
Kaye, David M.
Chin-Dusting, Jaye P. F.
Murphy, Andrew J.
High intraluminal pressure promotes vascular inflammation via caveolin-1
title High intraluminal pressure promotes vascular inflammation via caveolin-1
title_full High intraluminal pressure promotes vascular inflammation via caveolin-1
title_fullStr High intraluminal pressure promotes vascular inflammation via caveolin-1
title_full_unstemmed High intraluminal pressure promotes vascular inflammation via caveolin-1
title_short High intraluminal pressure promotes vascular inflammation via caveolin-1
title_sort high intraluminal pressure promotes vascular inflammation via caveolin-1
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7960707/
https://www.ncbi.nlm.nih.gov/pubmed/33723357
http://dx.doi.org/10.1038/s41598-021-85476-z
work_keys_str_mv AT michelldaniellel highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT shihatawaleda highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT andrewskarenl highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT abidinnurulaishazainal highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT jefferisannmaree highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT sampsonamandak highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT lumsdennatalieg highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT huetolivier highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT paratmarieodile highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT jenningsgarryl highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT partonrobertg highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT woollardkevinj highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT kayedavidm highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT chindustingjayepf highintraluminalpressurepromotesvascularinflammationviacaveolin1
AT murphyandrewj highintraluminalpressurepromotesvascularinflammationviacaveolin1