Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).

Abdominal aortic aneurysm (AAA), is a complex disorder characterized by vascular vessel wall remodeling. LIGHT (TNFSF14) is a proinflammatory cytokine associated with vascular disease. In the present study, the impact of genetic inactivation of Light was investigated in dissecting AAA induced by ang...

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Autores: Herrero-Cervera, A, Espinos-Estevez, C, Martin-Vano, S, Taberner-Cortes, A, Aguilar-Ballester, M, Vinue, A, Piqueras, L, Martinez-Hervas, S, Gonzalez-Navarro, H
Tipo de documento: artigo
Estado:Versão publicada
Data de publicação:2021
País:España
Recursos:INCLIVA
Repositório:r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
OAI Identifier:oai:incliva.fundanetsuite.com:p16343
Acesso em linha:https://incliva.portalinvestigacion.com/publicaciones/16343
Access Level:Acceso aberto
Palavra-chave:TNFSF14/LIGHT
abdominal aortic aneurysm
vascular smooth muscle cells
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spelling Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).Herrero-Cervera, AEspinos-Estevez, CMartin-Vano, STaberner-Cortes, AAguilar-Ballester, MVinue, APiqueras, LMartinez-Hervas, SGonzalez-Navarro, HTNFSF14/LIGHTabdominal aortic aneurysmvascular smooth muscle cellsAbdominal aortic aneurysm (AAA), is a complex disorder characterized by vascular vessel wall remodeling. LIGHT (TNFSF14) is a proinflammatory cytokine associated with vascular disease. In the present study, the impact of genetic inactivation of Light was investigated in dissecting AAA induced by angiotensin II (AngII) in the Apolipoprotein E-deficient (Apoe(-/-)) mice. Studies in aortic human (ah) vascular smooth muscle cells (VSMC) to study potential translation to human pathology were also performed. AngII-treated Apoe(-/-)Light(-/-) mice displayed increased abdominal aorta maximum diameter and AAA severity compared with Apoe(-/-) mice. Notably, reduced smooth muscle a-actin+ area and Acta2 and Col1a1 gene expression were observed in AAA from Apoe(-/-)Light(-/-) mice, suggesting a loss of VSMC contractile phenotype compared with controls. Decreased Opn and augmented Sox9 expression, which are associated with detrimental and non-contractile osteochondrogenic VSMC phenotypes, were also seen in AngII-treated Apoe(-/-)Light(-/-) mouse AAA. Consistent with a role of LIGHT preserving VSMC contractile characteristics, LIGHT-treatment of ahVSMCs diminished the expression of SOX9 and of the pluripotency marker CKIT. These effects were partly mediated through lymphotoxin ß receptor (LTßR) as the silencing of its gene ablated LIGHT effects on ahVSMCs. These studies suggest a protective role of LIGHT through mechanisms that prevent VSMC trans-differentiation in an LTßR-dependent manner.MDPI2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://incliva.portalinvestigacion.com/publicaciones/16343BiomedicinesISSN: 22279059reponame:r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVAinstname:INCLIVAInglésinfo:eu-repo/semantics/openAccessoai:incliva.fundanetsuite.com:p163432026-06-07T16:35:31Z
dc.title.none.fl_str_mv Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
title Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
spellingShingle Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
Herrero-Cervera, A
TNFSF14/LIGHT
abdominal aortic aneurysm
vascular smooth muscle cells
title_short Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
title_full Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
title_fullStr Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
title_full_unstemmed Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
title_sort Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).
dc.creator.none.fl_str_mv Herrero-Cervera, A
Espinos-Estevez, C
Martin-Vano, S
Taberner-Cortes, A
Aguilar-Ballester, M
Vinue, A
Piqueras, L
Martinez-Hervas, S
Gonzalez-Navarro, H
author Herrero-Cervera, A
author_facet Herrero-Cervera, A
Espinos-Estevez, C
Martin-Vano, S
Taberner-Cortes, A
Aguilar-Ballester, M
Vinue, A
Piqueras, L
Martinez-Hervas, S
Gonzalez-Navarro, H
author_role author
author2 Espinos-Estevez, C
Martin-Vano, S
Taberner-Cortes, A
Aguilar-Ballester, M
Vinue, A
Piqueras, L
Martinez-Hervas, S
Gonzalez-Navarro, H
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv TNFSF14/LIGHT
abdominal aortic aneurysm
vascular smooth muscle cells
topic TNFSF14/LIGHT
abdominal aortic aneurysm
vascular smooth muscle cells
description Abdominal aortic aneurysm (AAA), is a complex disorder characterized by vascular vessel wall remodeling. LIGHT (TNFSF14) is a proinflammatory cytokine associated with vascular disease. In the present study, the impact of genetic inactivation of Light was investigated in dissecting AAA induced by angiotensin II (AngII) in the Apolipoprotein E-deficient (Apoe(-/-)) mice. Studies in aortic human (ah) vascular smooth muscle cells (VSMC) to study potential translation to human pathology were also performed. AngII-treated Apoe(-/-)Light(-/-) mice displayed increased abdominal aorta maximum diameter and AAA severity compared with Apoe(-/-) mice. Notably, reduced smooth muscle a-actin+ area and Acta2 and Col1a1 gene expression were observed in AAA from Apoe(-/-)Light(-/-) mice, suggesting a loss of VSMC contractile phenotype compared with controls. Decreased Opn and augmented Sox9 expression, which are associated with detrimental and non-contractile osteochondrogenic VSMC phenotypes, were also seen in AngII-treated Apoe(-/-)Light(-/-) mouse AAA. Consistent with a role of LIGHT preserving VSMC contractile characteristics, LIGHT-treatment of ahVSMCs diminished the expression of SOX9 and of the pluripotency marker CKIT. These effects were partly mediated through lymphotoxin ß receptor (LTßR) as the silencing of its gene ablated LIGHT effects on ahVSMCs. These studies suggest a protective role of LIGHT through mechanisms that prevent VSMC trans-differentiation in an LTßR-dependent manner.
publishDate 2021
dc.date.none.fl_str_mv 2021
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://incliva.portalinvestigacion.com/publicaciones/16343
url https://incliva.portalinvestigacion.com/publicaciones/16343
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv Biomedicines
ISSN: 22279059
reponame:r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
instname:INCLIVA
instname_str INCLIVA
reponame_str r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
collection r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
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