Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats
- Autores
- Nakagawa, Pablo; Liu, Yunhe; Liao, Tang Dong; Chen, Xiaojuan; González, Germán Esteban; Bobbitt, Kevin R.; Smolarek, Derek; Peterson, Ed L.; Kedl, Ross; Yang, Xiao Ping; Rhaleb, Nour Eddine; Carretero, Oscar A.
- Año de publicación
- 2012
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs.
Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados Unidos
Fil: Liu, Yunhe. Henry Ford Hospital; Estados Unidos
Fil: Liao, Tang Dong. Henry Ford Hospital; Estados Unidos
Fil: Chen, Xiaojuan. Henry Ford Hospital; Estados Unidos
Fil: González, Germán Esteban. Henry Ford Hospital; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Bobbitt, Kevin R.. Henry Ford Hospital; Estados Unidos
Fil: Smolarek, Derek. Henry Ford Hospital; Estados Unidos
Fil: Peterson, Ed L.. Henry Ford Hospital; Estados Unidos
Fil: Kedl, Ross. University of Colorado; Estados Unidos
Fil: Yang, Xiao Ping. Henry Ford Hospital; Estados Unidos
Fil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados Unidos
Fil: Carretero, Oscar A.. Henry Ford Hospital; Estados Unidos - Materia
-
Cardiac Dysfunction
Cardiac Hypertrophy
Cd4+T Helper Lymphocytes
Delayed-Type Hypersensitivity
Experimental Autoimmune Myocarditis
N-Acetyl-Seryl-Aspartyl-Lysyl-Proline - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/67311
Ver los metadatos del registro completo
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Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in ratsNakagawa, PabloLiu, YunheLiao, Tang DongChen, XiaojuanGonzález, Germán EstebanBobbitt, Kevin R.Smolarek, DerekPeterson, Ed L.Kedl, RossYang, Xiao PingRhaleb, Nour EddineCarretero, Oscar A.Cardiac DysfunctionCardiac HypertrophyCd4+T Helper LymphocytesDelayed-Type HypersensitivityExperimental Autoimmune MyocarditisN-Acetyl-Seryl-Aspartyl-Lysyl-Prolinehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs.Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados UnidosFil: Liu, Yunhe. Henry Ford Hospital; Estados UnidosFil: Liao, Tang Dong. Henry Ford Hospital; Estados UnidosFil: Chen, Xiaojuan. Henry Ford Hospital; Estados UnidosFil: González, Germán Esteban. Henry Ford Hospital; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bobbitt, Kevin R.. Henry Ford Hospital; Estados UnidosFil: Smolarek, Derek. Henry Ford Hospital; Estados UnidosFil: Peterson, Ed L.. Henry Ford Hospital; Estados UnidosFil: Kedl, Ross. University of Colorado; Estados UnidosFil: Yang, Xiao Ping. Henry Ford Hospital; Estados UnidosFil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados UnidosFil: Carretero, Oscar A.. Henry Ford Hospital; Estados UnidosAmerican Physiological Society2012-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/67311Nakagawa, Pablo; Liu, Yunhe; Liao, Tang Dong; Chen, Xiaojuan; González, Germán Esteban; et al.; Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats; American Physiological Society; American Journal of Physiology - Heart and Circulatory Physiology; 303; 9; 11-2012; 1-140363-6135CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1152/ajpheart.00300.2011info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/full/10.1152/ajpheart.00300.2011info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:52:11Zoai:ri.conicet.gov.ar:11336/67311instacron: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 09:52:11.606CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
title |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
spellingShingle |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats Nakagawa, Pablo Cardiac Dysfunction Cardiac Hypertrophy Cd4+T Helper Lymphocytes Delayed-Type Hypersensitivity Experimental Autoimmune Myocarditis N-Acetyl-Seryl-Aspartyl-Lysyl-Proline |
title_short |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
title_full |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
title_fullStr |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
title_full_unstemmed |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
title_sort |
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats |
dc.creator.none.fl_str_mv |
Nakagawa, Pablo Liu, Yunhe Liao, Tang Dong Chen, Xiaojuan González, Germán Esteban Bobbitt, Kevin R. Smolarek, Derek Peterson, Ed L. Kedl, Ross Yang, Xiao Ping Rhaleb, Nour Eddine Carretero, Oscar A. |
author |
Nakagawa, Pablo |
author_facet |
Nakagawa, Pablo Liu, Yunhe Liao, Tang Dong Chen, Xiaojuan González, Germán Esteban Bobbitt, Kevin R. Smolarek, Derek Peterson, Ed L. Kedl, Ross Yang, Xiao Ping Rhaleb, Nour Eddine Carretero, Oscar A. |
author_role |
author |
author2 |
Liu, Yunhe Liao, Tang Dong Chen, Xiaojuan González, Germán Esteban Bobbitt, Kevin R. Smolarek, Derek Peterson, Ed L. Kedl, Ross Yang, Xiao Ping Rhaleb, Nour Eddine Carretero, Oscar A. |
author2_role |
author author author author author author author author author author author |
dc.subject.none.fl_str_mv |
Cardiac Dysfunction Cardiac Hypertrophy Cd4+T Helper Lymphocytes Delayed-Type Hypersensitivity Experimental Autoimmune Myocarditis N-Acetyl-Seryl-Aspartyl-Lysyl-Proline |
topic |
Cardiac Dysfunction Cardiac Hypertrophy Cd4+T Helper Lymphocytes Delayed-Type Hypersensitivity Experimental Autoimmune Myocarditis N-Acetyl-Seryl-Aspartyl-Lysyl-Proline |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs. Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados Unidos Fil: Liu, Yunhe. Henry Ford Hospital; Estados Unidos Fil: Liao, Tang Dong. Henry Ford Hospital; Estados Unidos Fil: Chen, Xiaojuan. Henry Ford Hospital; Estados Unidos Fil: González, Germán Esteban. Henry Ford Hospital; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Bobbitt, Kevin R.. Henry Ford Hospital; Estados Unidos Fil: Smolarek, Derek. Henry Ford Hospital; Estados Unidos Fil: Peterson, Ed L.. Henry Ford Hospital; Estados Unidos Fil: Kedl, Ross. University of Colorado; Estados Unidos Fil: Yang, Xiao Ping. Henry Ford Hospital; Estados Unidos Fil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados Unidos Fil: Carretero, Oscar A.. Henry Ford Hospital; Estados Unidos |
description |
Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs. |
publishDate |
2012 |
dc.date.none.fl_str_mv |
2012-11 |
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/11336/67311 Nakagawa, Pablo; Liu, Yunhe; Liao, Tang Dong; Chen, Xiaojuan; González, Germán Esteban; et al.; Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats; American Physiological Society; American Journal of Physiology - Heart and Circulatory Physiology; 303; 9; 11-2012; 1-14 0363-6135 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/67311 |
identifier_str_mv |
Nakagawa, Pablo; Liu, Yunhe; Liao, Tang Dong; Chen, Xiaojuan; González, Germán Esteban; et al.; Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats; American Physiological Society; American Journal of Physiology - Heart and Circulatory Physiology; 303; 9; 11-2012; 1-14 0363-6135 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpheart.00300.2011 info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/full/10.1152/ajpheart.00300.2011 |
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 |
American Physiological Society |
publisher.none.fl_str_mv |
American Physiological Society |
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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1842269142054338560 |
score |
13.13397 |