High intraluminal pressure promotes vascular inflammation via caveolin-1

Abstract 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....

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Autores principales:	Danielle L. Michell, Waled A. Shihata, Karen L. Andrews, Nurul Aisha Zainal Abidin, Ann-Maree Jefferis, Amanda K. Sampson, Natalie G. Lumsden, Olivier Huet, Marie-Odile Parat, Garry L. Jennings, Robert G. Parton, Kevin J. Woollard, David M. Kaye, Jaye P. F. Chin-Dusting, Andrew J. Murphy
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/89d56ef6af8740c7a60458ad31b61cc1
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spelling	oai:doaj.org-article:89d56ef6af8740c7a60458ad31b61cc12021-12-02T11:39:27ZHigh intraluminal pressure promotes vascular inflammation via caveolin-110.1038/s41598-021-85476-z2045-2322https://doaj.org/article/89d56ef6af8740c7a60458ad31b61cc12021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85476-zhttps://doaj.org/toc/2045-2322Abstract 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.Danielle L. MichellWaled A. ShihataKaren L. AndrewsNurul Aisha Zainal AbidinAnn-Maree JefferisAmanda K. SampsonNatalie G. LumsdenOlivier HuetMarie-Odile ParatGarry L. JenningsRobert G. PartonKevin J. WoollardDavid M. KayeJaye P. F. Chin-DustingAndrew J. MurphyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Danielle L. Michell Waled A. Shihata Karen L. Andrews Nurul Aisha Zainal Abidin Ann-Maree Jefferis Amanda K. Sampson Natalie G. Lumsden Olivier Huet Marie-Odile Parat Garry L. Jennings Robert G. Parton Kevin J. Woollard David M. Kaye Jaye P. F. Chin-Dusting Andrew J. Murphy High intraluminal pressure promotes vascular inflammation via caveolin-1
description	Abstract 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	article
author	Danielle L. Michell Waled A. Shihata Karen L. Andrews Nurul Aisha Zainal Abidin Ann-Maree Jefferis Amanda K. Sampson Natalie G. Lumsden Olivier Huet Marie-Odile Parat Garry L. Jennings Robert G. Parton Kevin J. Woollard David M. Kaye Jaye P. F. Chin-Dusting Andrew J. Murphy
author_facet	Danielle L. Michell Waled A. Shihata Karen L. Andrews Nurul Aisha Zainal Abidin Ann-Maree Jefferis Amanda K. Sampson Natalie G. Lumsden Olivier Huet Marie-Odile Parat Garry L. Jennings Robert G. Parton Kevin J. Woollard David M. Kaye Jaye P. F. Chin-Dusting Andrew J. Murphy
author_sort	Danielle L. Michell
title	High intraluminal pressure promotes vascular inflammation via caveolin-1
title_short	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_sort	high intraluminal pressure promotes vascular inflammation via caveolin-1
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/89d56ef6af8740c7a60458ad31b61cc1
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High intraluminal pressure promotes vascular inflammation via caveolin-1

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