Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.

Caveolae are omega-shaped plasma membrane micro-domains that are abundant in cells of the vascular system. Formation of caveolae depends on caveolin-1 and cavin-1 and lack of either protein leads to loss of caveolae. Mice with caveolin-1 deficiency have dysfunctional blood vessels, but whether absen...

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Autores principales:	Karl Swärd, Sebastian Albinsson, Catarina Rippe
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3e81187ff6b94cfeaa28a8b2732bfa49
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spelling	oai:doaj.org-article:3e81187ff6b94cfeaa28a8b2732bfa492021-11-18T08:26:43ZArterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.1932-620310.1371/journal.pone.0092428https://doaj.org/article/3e81187ff6b94cfeaa28a8b2732bfa492014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24658465/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Caveolae are omega-shaped plasma membrane micro-domains that are abundant in cells of the vascular system. Formation of caveolae depends on caveolin-1 and cavin-1 and lack of either protein leads to loss of caveolae. Mice with caveolin-1 deficiency have dysfunctional blood vessels, but whether absence of cavin-1 similarly leads to vascular dysfunction is not known. Here we addressed this hypothesis using small mesenteric arteries from cavin-1-deficient mice. Cavin-1-reporter staining was intense in mesenteric arteries, brain arterioles and elsewhere in the vascular system, with positive staining of both endothelial and smooth muscle cells. Arterial expression of cavin-1, -2 and -3 was reduced in knockout (KO) arteries as was expression of caveolin-1, -2 and -3. Caveolae were absent in the endothelial and smooth muscle layers of small mesenteric arteries as determined by electron microscopy. Arginase, a negative regulator of nitric oxide production, was elevated in cavin-1 deficient arteries as was contraction in response to the α1-adrenergic agonist cirazoline. Detailed assessment of vascular dimensions revealed increased media thickness and reduced distensibility, arguing that enhanced contraction was due to increased muscle mass. Contrasting with increased α1-adrenergic contraction, myogenic tone was essentially absent and this appeared to be due in part to increased nitric oxide production. Vasomotion was less frequent in the knock-out vessels. In keeping with the opposing influences on arterial resistance of increased agonist-induced contractility and reduced myogenic tone, arterial blood pressure was unchanged in vivo. We conclude that deficiency of cavin-1 affects the function of small arteries, but that opposing influences on arterial resistance balance each other such that systemic blood pressure in unstressed mice is well maintained.Karl SwärdSebastian AlbinssonCatarina RippePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 3, p e92428 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Karl Swärd Sebastian Albinsson Catarina Rippe Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
description	Caveolae are omega-shaped plasma membrane micro-domains that are abundant in cells of the vascular system. Formation of caveolae depends on caveolin-1 and cavin-1 and lack of either protein leads to loss of caveolae. Mice with caveolin-1 deficiency have dysfunctional blood vessels, but whether absence of cavin-1 similarly leads to vascular dysfunction is not known. Here we addressed this hypothesis using small mesenteric arteries from cavin-1-deficient mice. Cavin-1-reporter staining was intense in mesenteric arteries, brain arterioles and elsewhere in the vascular system, with positive staining of both endothelial and smooth muscle cells. Arterial expression of cavin-1, -2 and -3 was reduced in knockout (KO) arteries as was expression of caveolin-1, -2 and -3. Caveolae were absent in the endothelial and smooth muscle layers of small mesenteric arteries as determined by electron microscopy. Arginase, a negative regulator of nitric oxide production, was elevated in cavin-1 deficient arteries as was contraction in response to the α1-adrenergic agonist cirazoline. Detailed assessment of vascular dimensions revealed increased media thickness and reduced distensibility, arguing that enhanced contraction was due to increased muscle mass. Contrasting with increased α1-adrenergic contraction, myogenic tone was essentially absent and this appeared to be due in part to increased nitric oxide production. Vasomotion was less frequent in the knock-out vessels. In keeping with the opposing influences on arterial resistance of increased agonist-induced contractility and reduced myogenic tone, arterial blood pressure was unchanged in vivo. We conclude that deficiency of cavin-1 affects the function of small arteries, but that opposing influences on arterial resistance balance each other such that systemic blood pressure in unstressed mice is well maintained.
format	article
author	Karl Swärd Sebastian Albinsson Catarina Rippe
author_facet	Karl Swärd Sebastian Albinsson Catarina Rippe
author_sort	Karl Swärd
title	Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
title_short	Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
title_full	Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
title_fullStr	Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
title_full_unstemmed	Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
title_sort	arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/3e81187ff6b94cfeaa28a8b2732bfa49
work_keys_str_mv	AT karlsward arterialdysfunctionbutmaintainedsystemicbloodpressureincavin1deficientmice AT sebastianalbinsson arterialdysfunctionbutmaintainedsystemicbloodpressureincavin1deficientmice AT catarinarippe arterialdysfunctionbutmaintainedsystemicbloodpressureincavin1deficientmice
_version_	1718421796432117760

Arterial dysfunction but maintained systemic blood pressure in cavin-1-deficient mice.

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