Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction

Autores
Seropian, Ignacio Miguel; Cerliani, Juan Pablo; Toldo, Stefano; Van Tassell, Benjamín W.; Ilarregui, Juan Martin; González, Germán Esteban; Matoso, Mirian; Salloum, Fadi N.; Melchior, Ryan; Gelpi, Ricardo Jorge; Stupirski, Juan Carlos; Benatar, Alejandro Francisco; Gomez, Karina Andrea; Morales, Maria Celina; Abbate, Horacio Antonio; Rabinovich, Gabriel Adrián
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1-/-) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI. © 2013 American Society for Investigative Pathology.
Fil: Seropian, Ignacio Miguel. Virginia Commonwealth University; Estados Unidos
Fil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Toldo, Stefano. Virginia Commonwealth University; Estados Unidos
Fil: Van Tassell, Benjamín W.. Virginia Commonwealth University; Estados Unidos
Fil: Ilarregui, Juan Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Matoso, Mirian. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Salloum, Fadi N.. Virginia Commonwealth University; Estados Unidos
Fil: Melchior, Ryan. Virginia Commonwealth University; Estados Unidos
Fil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Morales, Maria Celina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Abbate, Horacio Antonio. Virginia Commonwealth University; Estados Unidos
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Materia
Galectin-1
Acute Myocardial Infarction
Inflammation
Cytokines
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:11336/76802
Acceder
id CONICETDig_e848e11fb276b4c93a86d29ee6a208fc
oai_identifier_str oai:ri.conicet.gov.ar:11336/76802
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarctionSeropian, Ignacio MiguelCerliani, Juan PabloToldo, StefanoVan Tassell, Benjamín W.Ilarregui, Juan MartinGonzález, Germán EstebanMatoso, MirianSalloum, Fadi N.Melchior, RyanGelpi, Ricardo JorgeStupirski, Juan CarlosBenatar, Alejandro FranciscoGomez, Karina AndreaMorales, Maria CelinaAbbate, Horacio AntonioRabinovich, Gabriel AdriánGalectin-1Acute Myocardial InfarctionInflammationCytokineshttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1-/-) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI. © 2013 American Society for Investigative Pathology.Fil: Seropian, Ignacio Miguel. Virginia Commonwealth University; Estados UnidosFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Toldo, Stefano. Virginia Commonwealth University; Estados UnidosFil: Van Tassell, Benjamín W.. Virginia Commonwealth University; Estados UnidosFil: Ilarregui, Juan Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Matoso, Mirian. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Salloum, Fadi N.. Virginia Commonwealth University; Estados UnidosFil: Melchior, Ryan. Virginia Commonwealth University; Estados UnidosFil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Morales, Maria Celina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Abbate, Horacio Antonio. Virginia Commonwealth University; Estados UnidosFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaAmerican Society of Investigative Pathology2013-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/76802Seropian, Ignacio Miguel; Cerliani, Juan Pablo; Toldo, Stefano; Van Tassell, Benjamín W.; Ilarregui, Juan Martin; et al.; Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction; American Society of Investigative Pathology; American Journal Of Pathology; 182; 1; 1-2013; 29-400002-9440CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.ajpath.2012.09.022info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0002944012007407info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:10:17Zoai:ri.conicet.gov.ar:11336/76802instacron: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:34982025-09-03 10:10:17.71CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
title Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
spellingShingle Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
Seropian, Ignacio Miguel
Galectin-1
Acute Myocardial Infarction
Inflammation
Cytokines
title_short Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
title_full Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
title_fullStr Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
title_full_unstemmed Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
title_sort Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction
dc.creator.none.fl_str_mv Seropian, Ignacio Miguel
Cerliani, Juan Pablo
Toldo, Stefano
Van Tassell, Benjamín W.
Ilarregui, Juan Martin
González, Germán Esteban
Matoso, Mirian
Salloum, Fadi N.
Melchior, Ryan
Gelpi, Ricardo Jorge
Stupirski, Juan Carlos
Benatar, Alejandro Francisco
Gomez, Karina Andrea
Morales, Maria Celina
Abbate, Horacio Antonio
Rabinovich, Gabriel Adrián
author Seropian, Ignacio Miguel
author_facet Seropian, Ignacio Miguel
Cerliani, Juan Pablo
Toldo, Stefano
Van Tassell, Benjamín W.
Ilarregui, Juan Martin
González, Germán Esteban
Matoso, Mirian
Salloum, Fadi N.
Melchior, Ryan
Gelpi, Ricardo Jorge
Stupirski, Juan Carlos
Benatar, Alejandro Francisco
Gomez, Karina Andrea
Morales, Maria Celina
Abbate, Horacio Antonio
Rabinovich, Gabriel Adrián
author_role author
author2 Cerliani, Juan Pablo
Toldo, Stefano
Van Tassell, Benjamín W.
Ilarregui, Juan Martin
González, Germán Esteban
Matoso, Mirian
Salloum, Fadi N.
Melchior, Ryan
Gelpi, Ricardo Jorge
Stupirski, Juan Carlos
Benatar, Alejandro Francisco
Gomez, Karina Andrea
Morales, Maria Celina
Abbate, Horacio Antonio
Rabinovich, Gabriel Adrián
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Galectin-1
Acute Myocardial Infarction
Inflammation
Cytokines
topic Galectin-1
Acute Myocardial Infarction
Inflammation
Cytokines
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1-/-) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI. © 2013 American Society for Investigative Pathology.
Fil: Seropian, Ignacio Miguel. Virginia Commonwealth University; Estados Unidos
Fil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Toldo, Stefano. Virginia Commonwealth University; Estados Unidos
Fil: Van Tassell, Benjamín W.. Virginia Commonwealth University; Estados Unidos
Fil: Ilarregui, Juan Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Matoso, Mirian. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Salloum, Fadi N.. Virginia Commonwealth University; Estados Unidos
Fil: Melchior, Ryan. Virginia Commonwealth University; Estados Unidos
Fil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Morales, Maria Celina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
Fil: Abbate, Horacio Antonio. Virginia Commonwealth University; Estados Unidos
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
description Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1-/-) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI. © 2013 American Society for Investigative Pathology.
publishDate 2013
dc.date.none.fl_str_mv 2013-01
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/11336/76802
Seropian, Ignacio Miguel; Cerliani, Juan Pablo; Toldo, Stefano; Van Tassell, Benjamín W.; Ilarregui, Juan Martin; et al.; Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction; American Society of Investigative Pathology; American Journal Of Pathology; 182; 1; 1-2013; 29-40
0002-9440
CONICET Digital
CONICET
url http://hdl.handle.net/11336/76802
identifier_str_mv Seropian, Ignacio Miguel; Cerliani, Juan Pablo; Toldo, Stefano; Van Tassell, Benjamín W.; Ilarregui, Juan Martin; et al.; Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction; American Society of Investigative Pathology; American Journal Of Pathology; 182; 1; 1-2013; 29-40
0002-9440
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S0002944012007407
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eu_rights_str_mv openAccess
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dc.publisher.none.fl_str_mv American Society of Investigative Pathology
publisher.none.fl_str_mv American Society of Investigative Pathology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
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reponame_str CONICET Digital (CONICET)
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repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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