Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice

Autores
Peng, Hongmei; Yang, Xiao Ping; Carretero, Oscar A.; Nakagawa, Pablo; D'Ambrosio, Martin; Leung, Pablo; Xu, Jiang; Peterson, Edward L.; González, Germán Esteban; Harding, Pamela; Rhaleb, Nour Eddine
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Balb/c mice, which are T-helper lymphocyte 2 (Th2) responders, are highly susceptible to infectious and non-infectious heart diseases, whereas C57BL/6 mice (Th1 responders) are not. Angiotensin II (Ang II) is not only a vasopressor but also a pro-inflammatory factor that leads to cardiac hypertrophy, fibrosis and dysfunction. We hypothesized that Ang II exacerbates cardiac damage in Balb/c but not in C57BL/6 mice even though both strains have a similar level of hypertension. Twelve-week-old male C57BL/6J and Balb/c mice received either vehicle or Ang II (1.4 mg kg -1 day -1, s.c. via osmotic minipump) for 8 weeks. At baseline, Balb/c mice exhibited the following: (1) a lower heart rate; (2) an enlarged left ventricular chamber; (3) a lower ejection fraction and shortening fraction; and (4) twice the left ventricular collagen deposition of age-matched C57BL/6J mice. Angiotensin II raised systolic blood pressure (to ~150 mmHg) and induced cardiomyocyte hypertrophy in a similar manner in both strains. While C57BL/6J mice developed compensatory concentric hypertrophy and fibrosis in response to Ang II, Balb/c mice demonstrated severe left ventricular chamber dilatation, wall thinning and fibrosis, leading to congestive heart failure as evidenced by dramatically decreased ejection fraction and lung congestion (significant increase in lung weight), which are both characteristic of dilated cardiomyopathy. Our study suggests that the Th phenotype plays an active role in cardiac remodelling and function both in basal conditions and in hypertension. Angiotensin II-induced dilated cardiomyopathy in Balb/c mice is an ideal animal model for studying the impact of the adaptive immune system on cardiac remodelling and function and for testing strategies to prevent or treat hypertension-associated heart failure. © 2011 The Authors. Journal compilation © 2011 The Physiological Society.
Fil: Peng, Hongmei. Henry Ford Hospital; Estados Unidos
Fil: Yang, Xiao Ping. Henry Ford Hospital; Estados Unidos
Fil: Carretero, Oscar A.. Henry Ford Hospital; Estados Unidos
Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados Unidos
Fil: D'Ambrosio, Martin. Henry Ford Hospital; Estados Unidos
Fil: Leung, Pablo. Henry Ford Hospital; Estados Unidos
Fil: Xu, Jiang. Henry Ford Hospital; Estados Unidos
Fil: Peterson, Edward L.. Henry Ford Hospital; Estados Unidos
Fil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Henry Ford Hospital; Estados Unidos
Fil: Harding, Pamela. Henry Ford Hospital; Estados Unidos
Fil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados Unidos
Materia
HYPERTENSION
ANGIOTENSIN II
IMMUNITY
VENTRICULAR FUNCTION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/67545
Acceder
id CONICETDig_8edd2e45ddecd6c640a28846eb6bc947
oai_identifier_str oai:ri.conicet.gov.ar:11336/67545
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J micePeng, HongmeiYang, Xiao PingCarretero, Oscar A.Nakagawa, PabloD'Ambrosio, MartinLeung, PabloXu, JiangPeterson, Edward L.González, Germán EstebanHarding, PamelaRhaleb, Nour EddineHYPERTENSIONANGIOTENSIN IIIMMUNITYVENTRICULAR FUNCTIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Balb/c mice, which are T-helper lymphocyte 2 (Th2) responders, are highly susceptible to infectious and non-infectious heart diseases, whereas C57BL/6 mice (Th1 responders) are not. Angiotensin II (Ang II) is not only a vasopressor but also a pro-inflammatory factor that leads to cardiac hypertrophy, fibrosis and dysfunction. We hypothesized that Ang II exacerbates cardiac damage in Balb/c but not in C57BL/6 mice even though both strains have a similar level of hypertension. Twelve-week-old male C57BL/6J and Balb/c mice received either vehicle or Ang II (1.4 mg kg -1 day -1, s.c. via osmotic minipump) for 8 weeks. At baseline, Balb/c mice exhibited the following: (1) a lower heart rate; (2) an enlarged left ventricular chamber; (3) a lower ejection fraction and shortening fraction; and (4) twice the left ventricular collagen deposition of age-matched C57BL/6J mice. Angiotensin II raised systolic blood pressure (to ~150 mmHg) and induced cardiomyocyte hypertrophy in a similar manner in both strains. While C57BL/6J mice developed compensatory concentric hypertrophy and fibrosis in response to Ang II, Balb/c mice demonstrated severe left ventricular chamber dilatation, wall thinning and fibrosis, leading to congestive heart failure as evidenced by dramatically decreased ejection fraction and lung congestion (significant increase in lung weight), which are both characteristic of dilated cardiomyopathy. Our study suggests that the Th phenotype plays an active role in cardiac remodelling and function both in basal conditions and in hypertension. Angiotensin II-induced dilated cardiomyopathy in Balb/c mice is an ideal animal model for studying the impact of the adaptive immune system on cardiac remodelling and function and for testing strategies to prevent or treat hypertension-associated heart failure. © 2011 The Authors. Journal compilation © 2011 The Physiological Society.Fil: Peng, Hongmei. Henry Ford Hospital; Estados UnidosFil: Yang, Xiao Ping. Henry Ford Hospital; Estados UnidosFil: Carretero, Oscar A.. Henry Ford Hospital; Estados UnidosFil: Nakagawa, Pablo. Henry Ford Hospital; Estados UnidosFil: D'Ambrosio, Martin. Henry Ford Hospital; Estados UnidosFil: Leung, Pablo. Henry Ford Hospital; Estados UnidosFil: Xu, Jiang. Henry Ford Hospital; Estados UnidosFil: Peterson, Edward L.. Henry Ford Hospital; Estados UnidosFil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Henry Ford Hospital; Estados UnidosFil: Harding, Pamela. Henry Ford Hospital; Estados UnidosFil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados UnidosWiley Blackwell Publishing, Inc2011-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/mswordapplication/pdfhttp://hdl.handle.net/11336/67545Peng, Hongmei; Yang, Xiao Ping; Carretero, Oscar A.; Nakagawa, Pablo; D'Ambrosio, Martin; et al.; Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice; Wiley Blackwell Publishing, Inc; Experimental Physiology; 96; 8; 8-2011; 756-7640958-0670CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1113/expphysiol.2011.057612info:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/expphysiol.2011.057612info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:36:11Zoai:ri.conicet.gov.ar:11336/67545instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:36:12.283CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
title Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
spellingShingle Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
Peng, Hongmei
HYPERTENSION
ANGIOTENSIN II
IMMUNITY
VENTRICULAR FUNCTION
title_short Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
title_full Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
title_fullStr Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
title_full_unstemmed Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
title_sort Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice
dc.creator.none.fl_str_mv Peng, Hongmei
Yang, Xiao Ping
Carretero, Oscar A.
Nakagawa, Pablo
D'Ambrosio, Martin
Leung, Pablo
Xu, Jiang
Peterson, Edward L.
González, Germán Esteban
Harding, Pamela
Rhaleb, Nour Eddine
author Peng, Hongmei
author_facet Peng, Hongmei
Yang, Xiao Ping
Carretero, Oscar A.
Nakagawa, Pablo
D'Ambrosio, Martin
Leung, Pablo
Xu, Jiang
Peterson, Edward L.
González, Germán Esteban
Harding, Pamela
Rhaleb, Nour Eddine
author_role author
author2 Yang, Xiao Ping
Carretero, Oscar A.
Nakagawa, Pablo
D'Ambrosio, Martin
Leung, Pablo
Xu, Jiang
Peterson, Edward L.
González, Germán Esteban
Harding, Pamela
Rhaleb, Nour Eddine
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv HYPERTENSION
ANGIOTENSIN II
IMMUNITY
VENTRICULAR FUNCTION
topic HYPERTENSION
ANGIOTENSIN II
IMMUNITY
VENTRICULAR FUNCTION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Balb/c mice, which are T-helper lymphocyte 2 (Th2) responders, are highly susceptible to infectious and non-infectious heart diseases, whereas C57BL/6 mice (Th1 responders) are not. Angiotensin II (Ang II) is not only a vasopressor but also a pro-inflammatory factor that leads to cardiac hypertrophy, fibrosis and dysfunction. We hypothesized that Ang II exacerbates cardiac damage in Balb/c but not in C57BL/6 mice even though both strains have a similar level of hypertension. Twelve-week-old male C57BL/6J and Balb/c mice received either vehicle or Ang II (1.4 mg kg -1 day -1, s.c. via osmotic minipump) for 8 weeks. At baseline, Balb/c mice exhibited the following: (1) a lower heart rate; (2) an enlarged left ventricular chamber; (3) a lower ejection fraction and shortening fraction; and (4) twice the left ventricular collagen deposition of age-matched C57BL/6J mice. Angiotensin II raised systolic blood pressure (to ~150 mmHg) and induced cardiomyocyte hypertrophy in a similar manner in both strains. While C57BL/6J mice developed compensatory concentric hypertrophy and fibrosis in response to Ang II, Balb/c mice demonstrated severe left ventricular chamber dilatation, wall thinning and fibrosis, leading to congestive heart failure as evidenced by dramatically decreased ejection fraction and lung congestion (significant increase in lung weight), which are both characteristic of dilated cardiomyopathy. Our study suggests that the Th phenotype plays an active role in cardiac remodelling and function both in basal conditions and in hypertension. Angiotensin II-induced dilated cardiomyopathy in Balb/c mice is an ideal animal model for studying the impact of the adaptive immune system on cardiac remodelling and function and for testing strategies to prevent or treat hypertension-associated heart failure. © 2011 The Authors. Journal compilation © 2011 The Physiological Society.
Fil: Peng, Hongmei. Henry Ford Hospital; Estados Unidos
Fil: Yang, Xiao Ping. Henry Ford Hospital; Estados Unidos
Fil: Carretero, Oscar A.. Henry Ford Hospital; Estados Unidos
Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados Unidos
Fil: D'Ambrosio, Martin. Henry Ford Hospital; Estados Unidos
Fil: Leung, Pablo. Henry Ford Hospital; Estados Unidos
Fil: Xu, Jiang. Henry Ford Hospital; Estados Unidos
Fil: Peterson, Edward L.. Henry Ford Hospital; Estados Unidos
Fil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Henry Ford Hospital; Estados Unidos
Fil: Harding, Pamela. Henry Ford Hospital; Estados Unidos
Fil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados Unidos
description Balb/c mice, which are T-helper lymphocyte 2 (Th2) responders, are highly susceptible to infectious and non-infectious heart diseases, whereas C57BL/6 mice (Th1 responders) are not. Angiotensin II (Ang II) is not only a vasopressor but also a pro-inflammatory factor that leads to cardiac hypertrophy, fibrosis and dysfunction. We hypothesized that Ang II exacerbates cardiac damage in Balb/c but not in C57BL/6 mice even though both strains have a similar level of hypertension. Twelve-week-old male C57BL/6J and Balb/c mice received either vehicle or Ang II (1.4 mg kg -1 day -1, s.c. via osmotic minipump) for 8 weeks. At baseline, Balb/c mice exhibited the following: (1) a lower heart rate; (2) an enlarged left ventricular chamber; (3) a lower ejection fraction and shortening fraction; and (4) twice the left ventricular collagen deposition of age-matched C57BL/6J mice. Angiotensin II raised systolic blood pressure (to ~150 mmHg) and induced cardiomyocyte hypertrophy in a similar manner in both strains. While C57BL/6J mice developed compensatory concentric hypertrophy and fibrosis in response to Ang II, Balb/c mice demonstrated severe left ventricular chamber dilatation, wall thinning and fibrosis, leading to congestive heart failure as evidenced by dramatically decreased ejection fraction and lung congestion (significant increase in lung weight), which are both characteristic of dilated cardiomyopathy. Our study suggests that the Th phenotype plays an active role in cardiac remodelling and function both in basal conditions and in hypertension. Angiotensin II-induced dilated cardiomyopathy in Balb/c mice is an ideal animal model for studying the impact of the adaptive immune system on cardiac remodelling and function and for testing strategies to prevent or treat hypertension-associated heart failure. © 2011 The Authors. Journal compilation © 2011 The Physiological Society.
publishDate 2011
dc.date.none.fl_str_mv 2011-08
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/67545
Peng, Hongmei; Yang, Xiao Ping; Carretero, Oscar A.; Nakagawa, Pablo; D'Ambrosio, Martin; et al.; Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice; Wiley Blackwell Publishing, Inc; Experimental Physiology; 96; 8; 8-2011; 756-764
0958-0670
CONICET Digital
CONICET
url http://hdl.handle.net/11336/67545
identifier_str_mv Peng, Hongmei; Yang, Xiao Ping; Carretero, Oscar A.; Nakagawa, Pablo; D'Ambrosio, Martin; et al.; Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice; Wiley Blackwell Publishing, Inc; Experimental Physiology; 96; 8; 8-2011; 756-764
0958-0670
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1113/expphysiol.2011.057612
info:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/expphysiol.2011.057612
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/msword
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1844613133670285312
score 13.070432

Publicaciones similares