NOD1 receptor is up-regulated in diabetic human and murine myocardium

Autores
Prieto, Patricia; Vallejo Cremades, María Teresa; Benito, Gemma; González Peramato, Pilar; Frances, Daniel Eleazar Antonio; Agra, Noelia; Terrón, Verónica; Gónzalez Ramos, Silvia; Delgado, Carmen; Ruiz Gayo, Mariano; Pacheco, Ivette; Velasco Martín, Juan P.; Regadera, Javier; Martín Sanz, Paloma; López Collazo, Eduardo; Boscá, Lisardo; Fernández Velasco, María
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Type 2 diabetes has a complex pathology that involves a chronic inflammatory state. Emerging evidence suggests a link between the innate immune system receptor NOD1 (nucleotide-binding and oligomerization domain 1) and the pathogenesis of diabetes, in monocytes and hepatic and adipose tissues. The aim of the present study was to assess the role of NOD1 in the progression of diabetic cardiomyopathy. We have measured NOD1 protein in cardiac tissue from Type 2 diabetic (db) mice. Heart and isolated cardiomyocytes from db mice revealed a significant increase in NOD1, together with an up-regulation of nuclear factor κB (NF-κB) and increased apoptosis. Heart tissue also exhibited an enhanced expression of pro-inflammatory cytokines. Selective NOD1 activation with C12-γ-D-glutamyl-m-diaminopimelic acid (iEDAP) resulted in an increased NF-κB activation and apoptosis, demonstrating the involvement of NOD1 both in wild-type and db mice. Moreover, HL-1 cardiomyocytes exposed to elevated concentrations of glucose plus palmitate displayed an enhanced NF-κB activity and apoptotic profile, which was prevented by silencing of NOD1 expression. To address this issue in human pathology, NOD1 expression was evaluated in myocardium obtained from patients with Type 2 diabetes (T2DMH) and from normoglycaemic individuals without cardiovascular histories (NH). We have found that NOD1 was expressed in both NH and T2DMH; however, NOD1 expression was significantly pronounced in T2DMH. Furthermore, both the pro-inflammatory cytokine tumour necrosis factor α (TNF-α) and the apoptosis mediator caspase-3 were up-regulated in T2DMH samples. Taken together, our results define an active role for NOD1 in the heightened inflammatory environment associated with both experimental and human diabetic cardiac disease.
Fil: Prieto, Patricia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Vallejo Cremades, María Teresa. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Benito, Gemma. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: González Peramato, Pilar. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Frances, Daniel Eleazar Antonio. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Rosario. Instituto de Fisiología Experimental (i); Argentina
Fil: Agra, Noelia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Terrón, Verónica. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Gónzalez Ramos, Silvia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Delgado, Carmen. Universidad Complutense de Madrid; España
Fil: Ruiz Gayo, Mariano . Universidad CEU San Pablo; España
Fil: Pacheco, Ivette. Hospital Militar de Managua; Nicaragua
Fil: Velasco Martín, Juan P.. Universidad Autónoma de Madrid; España
Fil: Regadera, Javier. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Martín Sanz, Paloma. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: López Collazo, Eduardo. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Boscá, Lisardo. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Fernández Velasco, María. Instituto de Investigacion Hospital Universitario La Paz; España
Materia
Apoptosis
Cardiomyocyte
Inflammation
Nucleotide-Binding And Oligomerization Domain 1 (Nod1)
Type 2 Diabetes
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:11336/6122
Acceder
id CONICETDig_ec1c99a23b5a0052822fc293a95d2ebd
oai_identifier_str oai:ri.conicet.gov.ar:11336/6122
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling NOD1 receptor is up-regulated in diabetic human and murine myocardiumPrieto, PatriciaVallejo Cremades, María TeresaBenito, GemmaGonzález Peramato, PilarFrances, Daniel Eleazar AntonioAgra, NoeliaTerrón, VerónicaGónzalez Ramos, SilviaDelgado, CarmenRuiz Gayo, Mariano Pacheco, IvetteVelasco Martín, Juan P.Regadera, JavierMartín Sanz, PalomaLópez Collazo, EduardoBoscá, LisardoFernández Velasco, MaríaApoptosisCardiomyocyteInflammationNucleotide-Binding And Oligomerization Domain 1 (Nod1)Type 2 Diabeteshttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Type 2 diabetes has a complex pathology that involves a chronic inflammatory state. Emerging evidence suggests a link between the innate immune system receptor NOD1 (nucleotide-binding and oligomerization domain 1) and the pathogenesis of diabetes, in monocytes and hepatic and adipose tissues. The aim of the present study was to assess the role of NOD1 in the progression of diabetic cardiomyopathy. We have measured NOD1 protein in cardiac tissue from Type 2 diabetic (db) mice. Heart and isolated cardiomyocytes from db mice revealed a significant increase in NOD1, together with an up-regulation of nuclear factor κB (NF-κB) and increased apoptosis. Heart tissue also exhibited an enhanced expression of pro-inflammatory cytokines. Selective NOD1 activation with C12-γ-D-glutamyl-m-diaminopimelic acid (iEDAP) resulted in an increased NF-κB activation and apoptosis, demonstrating the involvement of NOD1 both in wild-type and db mice. Moreover, HL-1 cardiomyocytes exposed to elevated concentrations of glucose plus palmitate displayed an enhanced NF-κB activity and apoptotic profile, which was prevented by silencing of NOD1 expression. To address this issue in human pathology, NOD1 expression was evaluated in myocardium obtained from patients with Type 2 diabetes (T2DMH) and from normoglycaemic individuals without cardiovascular histories (NH). We have found that NOD1 was expressed in both NH and T2DMH; however, NOD1 expression was significantly pronounced in T2DMH. Furthermore, both the pro-inflammatory cytokine tumour necrosis factor α (TNF-α) and the apoptosis mediator caspase-3 were up-regulated in T2DMH samples. Taken together, our results define an active role for NOD1 in the heightened inflammatory environment associated with both experimental and human diabetic cardiac disease.Fil: Prieto, Patricia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; EspañaFil: Vallejo Cremades, María Teresa. Instituto de Investigacion Hospital Universitario La Paz; EspañaFil: Benito, Gemma. Instituto de Investigacion Hospital Universitario La Paz; EspañaFil: González Peramato, Pilar. Instituto de Investigacion Hospital Universitario La Paz; EspañaFil: Frances, Daniel Eleazar Antonio. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Rosario. Instituto de Fisiología Experimental (i); ArgentinaFil: Agra, Noelia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; EspañaFil: Terrón, Verónica. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; EspañaFil: Gónzalez Ramos, Silvia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; EspañaFil: Delgado, Carmen. Universidad Complutense de Madrid; EspañaFil: Ruiz Gayo, Mariano . Universidad CEU San Pablo; EspañaFil: Pacheco, Ivette. Hospital Militar de Managua; NicaraguaFil: Velasco Martín, Juan P.. Universidad Autónoma de Madrid; EspañaFil: Regadera, Javier. Instituto de Investigacion Hospital Universitario La Paz; EspañaFil: Martín Sanz, Paloma. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; EspañaFil: López Collazo, Eduardo. Instituto de Investigacion Hospital Universitario La Paz; EspañaFil: Boscá, Lisardo. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; EspañaFil: Fernández Velasco, María. Instituto de Investigacion Hospital Universitario La Paz; EspañaPortland Press2014-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/6122Prieto, Patricia; Vallejo Cremades, María Teresa; Benito, Gemma; González Peramato, Pilar; Frances, Daniel Eleazar Antonio; et al.; NOD1 receptor is up-regulated in diabetic human and murine myocardium; Portland Press; Clinical Science; 127; 12; 12-2014; 665-6770143-5221enginfo:eu-repo/semantics/altIdentifier/url/http://www.clinsci.org/content/127/12/665.longinfo:eu-repo/semantics/altIdentifier/doi/info:eu-repo/semantics/altIdentifier/doi/10.1042/CS20140180info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:00:36Zoai:ri.conicet.gov.ar:11336/6122instacron: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 10:00:36.248CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv NOD1 receptor is up-regulated in diabetic human and murine myocardium
title NOD1 receptor is up-regulated in diabetic human and murine myocardium
spellingShingle NOD1 receptor is up-regulated in diabetic human and murine myocardium
Prieto, Patricia
Apoptosis
Cardiomyocyte
Inflammation
Nucleotide-Binding And Oligomerization Domain 1 (Nod1)
Type 2 Diabetes
title_short NOD1 receptor is up-regulated in diabetic human and murine myocardium
title_full NOD1 receptor is up-regulated in diabetic human and murine myocardium
title_fullStr NOD1 receptor is up-regulated in diabetic human and murine myocardium
title_full_unstemmed NOD1 receptor is up-regulated in diabetic human and murine myocardium
title_sort NOD1 receptor is up-regulated in diabetic human and murine myocardium
dc.creator.none.fl_str_mv Prieto, Patricia
Vallejo Cremades, María Teresa
Benito, Gemma
González Peramato, Pilar
Frances, Daniel Eleazar Antonio
Agra, Noelia
Terrón, Verónica
Gónzalez Ramos, Silvia
Delgado, Carmen
Ruiz Gayo, Mariano
Pacheco, Ivette
Velasco Martín, Juan P.
Regadera, Javier
Martín Sanz, Paloma
López Collazo, Eduardo
Boscá, Lisardo
Fernández Velasco, María
author Prieto, Patricia
author_facet Prieto, Patricia
Vallejo Cremades, María Teresa
Benito, Gemma
González Peramato, Pilar
Frances, Daniel Eleazar Antonio
Agra, Noelia
Terrón, Verónica
Gónzalez Ramos, Silvia
Delgado, Carmen
Ruiz Gayo, Mariano
Pacheco, Ivette
Velasco Martín, Juan P.
Regadera, Javier
Martín Sanz, Paloma
López Collazo, Eduardo
Boscá, Lisardo
Fernández Velasco, María
author_role author
author2 Vallejo Cremades, María Teresa
Benito, Gemma
González Peramato, Pilar
Frances, Daniel Eleazar Antonio
Agra, Noelia
Terrón, Verónica
Gónzalez Ramos, Silvia
Delgado, Carmen
Ruiz Gayo, Mariano
Pacheco, Ivette
Velasco Martín, Juan P.
Regadera, Javier
Martín Sanz, Paloma
López Collazo, Eduardo
Boscá, Lisardo
Fernández Velasco, María
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Apoptosis
Cardiomyocyte
Inflammation
Nucleotide-Binding And Oligomerization Domain 1 (Nod1)
Type 2 Diabetes
topic Apoptosis
Cardiomyocyte
Inflammation
Nucleotide-Binding And Oligomerization Domain 1 (Nod1)
Type 2 Diabetes
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Type 2 diabetes has a complex pathology that involves a chronic inflammatory state. Emerging evidence suggests a link between the innate immune system receptor NOD1 (nucleotide-binding and oligomerization domain 1) and the pathogenesis of diabetes, in monocytes and hepatic and adipose tissues. The aim of the present study was to assess the role of NOD1 in the progression of diabetic cardiomyopathy. We have measured NOD1 protein in cardiac tissue from Type 2 diabetic (db) mice. Heart and isolated cardiomyocytes from db mice revealed a significant increase in NOD1, together with an up-regulation of nuclear factor κB (NF-κB) and increased apoptosis. Heart tissue also exhibited an enhanced expression of pro-inflammatory cytokines. Selective NOD1 activation with C12-γ-D-glutamyl-m-diaminopimelic acid (iEDAP) resulted in an increased NF-κB activation and apoptosis, demonstrating the involvement of NOD1 both in wild-type and db mice. Moreover, HL-1 cardiomyocytes exposed to elevated concentrations of glucose plus palmitate displayed an enhanced NF-κB activity and apoptotic profile, which was prevented by silencing of NOD1 expression. To address this issue in human pathology, NOD1 expression was evaluated in myocardium obtained from patients with Type 2 diabetes (T2DMH) and from normoglycaemic individuals without cardiovascular histories (NH). We have found that NOD1 was expressed in both NH and T2DMH; however, NOD1 expression was significantly pronounced in T2DMH. Furthermore, both the pro-inflammatory cytokine tumour necrosis factor α (TNF-α) and the apoptosis mediator caspase-3 were up-regulated in T2DMH samples. Taken together, our results define an active role for NOD1 in the heightened inflammatory environment associated with both experimental and human diabetic cardiac disease.
Fil: Prieto, Patricia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Vallejo Cremades, María Teresa. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Benito, Gemma. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: González Peramato, Pilar. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Frances, Daniel Eleazar Antonio. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Rosario. Instituto de Fisiología Experimental (i); Argentina
Fil: Agra, Noelia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Terrón, Verónica. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Gónzalez Ramos, Silvia. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Delgado, Carmen. Universidad Complutense de Madrid; España
Fil: Ruiz Gayo, Mariano . Universidad CEU San Pablo; España
Fil: Pacheco, Ivette. Hospital Militar de Managua; Nicaragua
Fil: Velasco Martín, Juan P.. Universidad Autónoma de Madrid; España
Fil: Regadera, Javier. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Martín Sanz, Paloma. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: López Collazo, Eduardo. Instituto de Investigacion Hospital Universitario La Paz; España
Fil: Boscá, Lisardo. Consejo Superior de Investigaciones Científicas. Instituto de Investigaciones Biomedicas Alberto Sols; España
Fil: Fernández Velasco, María. Instituto de Investigacion Hospital Universitario La Paz; España
description Type 2 diabetes has a complex pathology that involves a chronic inflammatory state. Emerging evidence suggests a link between the innate immune system receptor NOD1 (nucleotide-binding and oligomerization domain 1) and the pathogenesis of diabetes, in monocytes and hepatic and adipose tissues. The aim of the present study was to assess the role of NOD1 in the progression of diabetic cardiomyopathy. We have measured NOD1 protein in cardiac tissue from Type 2 diabetic (db) mice. Heart and isolated cardiomyocytes from db mice revealed a significant increase in NOD1, together with an up-regulation of nuclear factor κB (NF-κB) and increased apoptosis. Heart tissue also exhibited an enhanced expression of pro-inflammatory cytokines. Selective NOD1 activation with C12-γ-D-glutamyl-m-diaminopimelic acid (iEDAP) resulted in an increased NF-κB activation and apoptosis, demonstrating the involvement of NOD1 both in wild-type and db mice. Moreover, HL-1 cardiomyocytes exposed to elevated concentrations of glucose plus palmitate displayed an enhanced NF-κB activity and apoptotic profile, which was prevented by silencing of NOD1 expression. To address this issue in human pathology, NOD1 expression was evaluated in myocardium obtained from patients with Type 2 diabetes (T2DMH) and from normoglycaemic individuals without cardiovascular histories (NH). We have found that NOD1 was expressed in both NH and T2DMH; however, NOD1 expression was significantly pronounced in T2DMH. Furthermore, both the pro-inflammatory cytokine tumour necrosis factor α (TNF-α) and the apoptosis mediator caspase-3 were up-regulated in T2DMH samples. Taken together, our results define an active role for NOD1 in the heightened inflammatory environment associated with both experimental and human diabetic cardiac disease.
publishDate 2014
dc.date.none.fl_str_mv 2014-12
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/11336/6122
Prieto, Patricia; Vallejo Cremades, María Teresa; Benito, Gemma; González Peramato, Pilar; Frances, Daniel Eleazar Antonio; et al.; NOD1 receptor is up-regulated in diabetic human and murine myocardium; Portland Press; Clinical Science; 127; 12; 12-2014; 665-677
0143-5221
url http://hdl.handle.net/11336/6122
identifier_str_mv Prieto, Patricia; Vallejo Cremades, María Teresa; Benito, Gemma; González Peramato, Pilar; Frances, Daniel Eleazar Antonio; et al.; NOD1 receptor is up-regulated in diabetic human and murine myocardium; Portland Press; Clinical Science; 127; 12; 12-2014; 665-677
0143-5221
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.clinsci.org/content/127/12/665.long
info:eu-repo/semantics/altIdentifier/doi/
info:eu-repo/semantics/altIdentifier/doi/10.1042/CS20140180
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/pdf
dc.publisher.none.fl_str_mv Portland Press
publisher.none.fl_str_mv Portland Press
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
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score 13.13397

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