Dual Role of Thrombospondin-1 in Flow-Induced Remodeling

(1) Background: Chronic increases in blood flow, as in cardiovascular diseases, induce outward arterial remodeling. Thrombospondin-1 (TSP-1) is known to interact with matrix proteins and immune cell-surface receptors, but its contribution to flow-mediated remodeling in the microcirculation remains u...

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Autores principales:	Céline Grenier, Antoine Caillon, Mathilde Munier, Linda Grimaud, Tristan Champin, Bertrand Toutain, Céline Fassot, Olivier Blanc-Brude, Laurent Loufrani
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	thrombospondin-1 blood flow remodeling resistance arteries immune cells Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/0cdbcaa5ad6646fbb1fb700f30c4ef4d
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spelling	oai:doaj.org-article:0cdbcaa5ad6646fbb1fb700f30c4ef4d2021-11-11T17:28:33ZDual Role of Thrombospondin-1 in Flow-Induced Remodeling10.3390/ijms2221120861422-00671661-6596https://doaj.org/article/0cdbcaa5ad6646fbb1fb700f30c4ef4d2021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/12086https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067(1) Background: Chronic increases in blood flow, as in cardiovascular diseases, induce outward arterial remodeling. Thrombospondin-1 (TSP-1) is known to interact with matrix proteins and immune cell-surface receptors, but its contribution to flow-mediated remodeling in the microcirculation remains unknown. (2) Methods: Mesenteric arteries were ligated in vivo to generate high- (HF) and normal-flow (NF) arteries in wild-type (WT) and TSP-1-deleted mice (TSP-1<sup>−/−</sup>). After 7 days, arteries were isolated and studied ex vivo. (3) Results: Chronic increases in blood flow induced outward remodeling in WT mice (increasing diameter from 221 ± 10 to 280 ± 10 µm with 75 mmHg intraluminal pressure) without significant effect in TSP-1<sup>−/−</sup> (296 ± 18 to 303 ± 14 µm), neutropenic or adoptive bone marrow transfer mice. Four days after ligature, pro inflammatory gene expression levels (CD68, Cox2, Gp91phox, p47phox and p22phox) increased in WT HF arteries but not in TSP-1<sup>−/−</sup> mice. Perivascular neutrophil accumulation at day 4 was significantly lower in TSP-1<sup>−/−</sup> than in WT mice. (4) Conclusions: TSP-1 origin is important; indeed, circulating TSP-1 participates in vasodilation, whereas both circulating and tissue TSP-1 are involved in arterial wall thickness and diameter expansion.Céline GrenierAntoine CaillonMathilde MunierLinda GrimaudTristan ChampinBertrand ToutainCéline FassotOlivier Blanc-BrudeLaurent LoufraniMDPI AGarticlethrombospondin-1blood flowremodelingresistance arteriesimmune cellsBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12086, p 12086 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	thrombospondin-1 blood flow remodeling resistance arteries immune cells Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	thrombospondin-1 blood flow remodeling resistance arteries immune cells Biology (General) QH301-705.5 Chemistry QD1-999 Céline Grenier Antoine Caillon Mathilde Munier Linda Grimaud Tristan Champin Bertrand Toutain Céline Fassot Olivier Blanc-Brude Laurent Loufrani Dual Role of Thrombospondin-1 in Flow-Induced Remodeling
description	(1) Background: Chronic increases in blood flow, as in cardiovascular diseases, induce outward arterial remodeling. Thrombospondin-1 (TSP-1) is known to interact with matrix proteins and immune cell-surface receptors, but its contribution to flow-mediated remodeling in the microcirculation remains unknown. (2) Methods: Mesenteric arteries were ligated in vivo to generate high- (HF) and normal-flow (NF) arteries in wild-type (WT) and TSP-1-deleted mice (TSP-1<sup>−/−</sup>). After 7 days, arteries were isolated and studied ex vivo. (3) Results: Chronic increases in blood flow induced outward remodeling in WT mice (increasing diameter from 221 ± 10 to 280 ± 10 µm with 75 mmHg intraluminal pressure) without significant effect in TSP-1<sup>−/−</sup> (296 ± 18 to 303 ± 14 µm), neutropenic or adoptive bone marrow transfer mice. Four days after ligature, pro inflammatory gene expression levels (CD68, Cox2, Gp91phox, p47phox and p22phox) increased in WT HF arteries but not in TSP-1<sup>−/−</sup> mice. Perivascular neutrophil accumulation at day 4 was significantly lower in TSP-1<sup>−/−</sup> than in WT mice. (4) Conclusions: TSP-1 origin is important; indeed, circulating TSP-1 participates in vasodilation, whereas both circulating and tissue TSP-1 are involved in arterial wall thickness and diameter expansion.
format	article
author	Céline Grenier Antoine Caillon Mathilde Munier Linda Grimaud Tristan Champin Bertrand Toutain Céline Fassot Olivier Blanc-Brude Laurent Loufrani
author_facet	Céline Grenier Antoine Caillon Mathilde Munier Linda Grimaud Tristan Champin Bertrand Toutain Céline Fassot Olivier Blanc-Brude Laurent Loufrani
author_sort	Céline Grenier
title	Dual Role of Thrombospondin-1 in Flow-Induced Remodeling
title_short	Dual Role of Thrombospondin-1 in Flow-Induced Remodeling
title_full	Dual Role of Thrombospondin-1 in Flow-Induced Remodeling
title_fullStr	Dual Role of Thrombospondin-1 in Flow-Induced Remodeling
title_full_unstemmed	Dual Role of Thrombospondin-1 in Flow-Induced Remodeling
title_sort	dual role of thrombospondin-1 in flow-induced remodeling
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/0cdbcaa5ad6646fbb1fb700f30c4ef4d
work_keys_str_mv	AT celinegrenier dualroleofthrombospondin1inflowinducedremodeling AT antoinecaillon dualroleofthrombospondin1inflowinducedremodeling AT mathildemunier dualroleofthrombospondin1inflowinducedremodeling AT lindagrimaud dualroleofthrombospondin1inflowinducedremodeling AT tristanchampin dualroleofthrombospondin1inflowinducedremodeling AT bertrandtoutain dualroleofthrombospondin1inflowinducedremodeling AT celinefassot dualroleofthrombospondin1inflowinducedremodeling AT olivierblancbrude dualroleofthrombospondin1inflowinducedremodeling AT laurentloufrani dualroleofthrombospondin1inflowinducedremodeling
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Dual Role of Thrombospondin-1 in Flow-Induced Remodeling

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