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dc.contributor.author
Donato, Pablo Martín
dc.contributor.author
Buchholz, Bruno
dc.contributor.author
Morales, Celina
dc.contributor.author
Valdez, Laura Batriz
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Zaobornyj, Tamara
dc.contributor.author
Baratta, Sergio
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Paez, Diamela T.
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Matoso, Mirian
dc.contributor.author
Vaccarino, Guillermo
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Chejtman, Demian
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Agüero, Oscar
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Telayna, Juan
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Navia, José
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Hita, Alejandro
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Boveris, Alberto Antonio
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Gelpi, Ricardo Jorge
dc.date.available
2018-06-05T20:21:08Z
dc.date.issued
2017-03
dc.identifier.citation
Donato, Pablo Martín; Buchholz, Bruno; Morales, Celina; Valdez, Laura Batriz; Zaobornyj, Tamara; et al.; Loss of dystrophin is associated with increased myocardial stiffness in a model of left ventricular hypertrophy; Springer; Molecular and Cellular Biochemistry; 432; 1-2; 3-2017; 169-178
dc.identifier.issn
0300-8177
dc.identifier.uri
http://hdl.handle.net/11336/47390
dc.description.abstract
Transition from compensated to decompensated left ventricular hypertrophy (LVH) is accompanied by functional and structural changes. Here, the aim was to evaluate dystrophin expression in murine models and human subjects with LVH by transverse aortic constriction (TAC) and aortic stenosis (AS), respectively. We determined whether doxycycline (Doxy) prevented dystrophin expression and myocardial stiffness in mice. Additionally, ventricular function recovery was evaluated in patients 1 year after surgery. Mice were subjected to TAC and monitored for 3 weeks. A second group received Doxy treatment after TAC. Patients with AS were stratified by normal left ventricular end-diastolic wall stress (LVEDWS) and high LVEDWS, and groups were compared. In mice, LVH decreased inotropism and increased myocardial stiffness associated with a dystrophin breakdown and a decreased mitochondrial O2 uptake (MitoMVO2). These alterations were attenuated by Doxy. Patients with high LVEDWS showed similar results to those observed in mice. A correlation between dystrophin and myocardial stiffness was observed in both mice and humans. Systolic function at 1 year post-surgery was only recovered in the normal-LVEDWS group. In summary, mice and humans present diastolic dysfunction associated with dystrophin degradation. The recovery of ventricular function was observed only in patients with normal LVEDWS and without dystrophin degradation. In mice, Doxy improved MitoMVO2. Based on our results it is concluded that the LVH with high LVEDWS is associated to a degradation of dystrophin and increase of myocardial stiffness. At least in a murine model these alterations were attenuated after the administration of a matrix metalloprotease inhibitor.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Estenosis Aortica
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Diastole
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Ratones
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Pacientes
dc.subject.classification
Inmunología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Loss of dystrophin is associated with increased myocardial stiffness in a model of left ventricular hypertrophy
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-06-04T21:16:47Z
dc.identifier.eissn
1573-4919
dc.journal.volume
432
dc.journal.number
1-2
dc.journal.pagination
169-178
dc.journal.pais
Alemania
dc.journal.ciudad
Berlin
dc.description.fil
Fil: Donato, Pablo Martín. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Buchholz, Bruno. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Morales, Celina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
dc.description.fil
Fil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
dc.description.fil
Fil: Zaobornyj, Tamara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
dc.description.fil
Fil: Baratta, Sergio. Hospital Austral; Argentina
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Fil: Paez, Diamela T.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
dc.description.fil
Fil: Matoso, Mirian. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
dc.description.fil
Fil: Vaccarino, Guillermo. Hospital Austral; Argentina
dc.description.fil
Fil: Chejtman, Demian. Hospital Austral; Argentina
dc.description.fil
Fil: Agüero, Oscar. Hospital Austral; Argentina
dc.description.fil
Fil: Telayna, Juan. Hospital Austral; Argentina
dc.description.fil
Fil: Navia, José. Hospital Austral; Argentina
dc.description.fil
Fil: Hita, Alejandro. Hospital Austral; Argentina
dc.description.fil
Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina
dc.description.fil
Fil: Gelpi, Ricardo Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.journal.title
Molecular and Cellular Biochemistry
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1007/s11010-017-3007-z
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-017-3007-z


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