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dc.contributor.author
Nakagawa, Pablo
dc.contributor.author
Liu, Yunhe
dc.contributor.author
Liao, Tang Dong
dc.contributor.author
Chen, Xiaojuan
dc.contributor.author
González, Germán Esteban
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dc.contributor.author
Bobbitt, Kevin R.
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Smolarek, Derek
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Peterson, Ed L.
dc.contributor.author
Kedl, Ross
dc.contributor.author
Yang, Xiao Ping
dc.contributor.author
Rhaleb, Nour Eddine
dc.contributor.author
Carretero, Oscar A.
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dc.date.available
2019-01-03T18:59:05Z
dc.date.issued
2012-11
dc.identifier.citation
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
dc.identifier.issn
0363-6135
dc.identifier.uri
http://hdl.handle.net/11336/67311
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Physiological Society
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Cardiac Dysfunction
dc.subject
Cardiac Hypertrophy
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Cd4+T Helper Lymphocytes
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Delayed-Type Hypersensitivity
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Experimental Autoimmune Myocarditis
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N-Acetyl-Seryl-Aspartyl-Lysyl-Proline
dc.subject.classification
Fisiología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-01-02T19:39:16Z
dc.journal.volume
303
dc.journal.number
9
dc.journal.pagination
1-14
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Bethesda
dc.description.fil
Fil: Nakagawa, Pablo. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Liu, Yunhe. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Liao, Tang Dong. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Chen, Xiaojuan. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: González, Germán Esteban. Henry Ford Hospital; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Bobbitt, Kevin R.. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Smolarek, Derek. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Peterson, Ed L.. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Kedl, Ross. University of Colorado; Estados Unidos
dc.description.fil
Fil: Yang, Xiao Ping. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Rhaleb, Nour Eddine. Henry Ford Hospital; Estados Unidos
dc.description.fil
Fil: Carretero, Oscar A.. Henry Ford Hospital; Estados Unidos
dc.journal.title
American Journal of Physiology - Heart and Circulatory Physiology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/ajpheart.00300.2011
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/full/10.1152/ajpheart.00300.2011
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