Studies on the role of apoptosis after transient myocardial
ischemia: genetic deletion of the executioner caspases-3 and -7
does not limit infarct size and ventricular remodeling
Author
dc.contributor.author
Inserte, Javier
Author
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Cardona, María
Author
dc.contributor.author
Poncelas Nozal, Marcos
Author
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Hernando, Víctor
Author
dc.contributor.author
Vilardosa, Úrsula
Author
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Aluja, David
Author
dc.contributor.author
Parra, Víctor M.
Author
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Sanchis, Daniel
Author
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García Dorado, David
Admission date
dc.date.accessioned
2019-03-18T11:53:47Z
Available date
dc.date.available
2019-03-18T11:53:47Z
Publication date
dc.date.issued
2016
Cita de ítem
dc.identifier.citation
Basic Res Cardiol (2016) 111:18
Identifier
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14351803
Identifier
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03008428
Identifier
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10.1007/s00395-016-0537-6
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/166740
Abstract
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Although it is widely accepted that apoptosis
may contribute to cell death in myocardial infarction,
experimental evidence suggests that adult cardiomyocytes
repress the expression of the caspase-dependent apoptotic
pathway. The aim of this study was to analyze the contribution
of caspase-mediated apoptosis to myocardial
ischemia-reperfusion injury. Cardiac-specific caspase-3
deficient/full caspase-7-deficient mice (Casp3/7DKO) and
wild type control mice (WT) were subjected to in situ
ischemia by left anterior coronary artery ligation for
45 min followed by 24 h or 28 days of reperfusion. Heart
function was assessed using M-mode echocardiography.
Deletion of caspases did not modify neither infarct size
determined by triphenyltetrazolium staining after 24 h of
reperfusion (40.0 ± 5.1 % in WT vs. 36.2 ± 3.6 % in
Casp3/7DKO), nor the scar area measured by pricosirius
red staining after 28 days of reperfusion (41.1 ± 5.4 % in
WT vs. 44.6 ± 8.7 % in Casp3/7DKO). Morphometric and
echocardiographic studies performed 28 days after the
ischemic insult revealed left ventricular dilation and severe
cardiac dysfunction without statistically significant differences
between WT and Casp3/7DKO groups. These data
demonstrate that the executioner caspases-3 and -7 do not
significantly contribute to cardiomyocyte death induced by
transient coronary occlusion and provide the first evidence
obtained in an in vivo model that argues against a relevant
role of apoptosis through the canonical caspase pathway in
this context.
Studies on the role of apoptosis after transient myocardial
ischemia: genetic deletion of the executioner caspases-3 and -7
does not limit infarct size and ventricular remodeling