Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.

Diabetes is associated with higher incidence of myocardial infarction (MI) and increased propensity for subsequent events post-MI. Here we conducted a temporal analysis of the influence of diabetes on cardiac dysfunction and remodeling after ischemia reperfusion (IR) injury in mice. Diabetes was ind...

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Autores principales: Megumi Eguchi, Young Hwa Kim, Keon Wook Kang, Chi Young Shim, Yangsoo Jang, Thierry Dorval, Kwang Joon Kim, Gary Sweeney
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Publicado: Public Library of Science (PLoS) 2012
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Acceso en línea:https://doaj.org/article/f90ba337ddc349d187ea71a2d58db1b0
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spelling oai:doaj.org-article:f90ba337ddc349d187ea71a2d58db1b02021-11-18T07:28:43ZIschemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.1932-620310.1371/journal.pone.0030450https://doaj.org/article/f90ba337ddc349d187ea71a2d58db1b02012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22347376/?tool=EBIhttps://doaj.org/toc/1932-6203Diabetes is associated with higher incidence of myocardial infarction (MI) and increased propensity for subsequent events post-MI. Here we conducted a temporal analysis of the influence of diabetes on cardiac dysfunction and remodeling after ischemia reperfusion (IR) injury in mice. Diabetes was induced using streptozotocin and IR performed by ligating the left anterior descending coronary artery for 30 min followed by reperfusion for up to 42 days. We first evaluated changes in cardiac function using echocardiography after 24 hours reperfusion and observed IR injury significantly decreased the systolic function, such as ejection fraction, fractional shortening and end systolic left ventricular volume (LVESV) in both control and diabetic mice. The longitudinal systolic and diastolic strain rate were altered after IR, but there were no significant differences between diabetic mice and controls. However, a reduced ability to metabolize glucose was observed in the diabetic animals as determined by PET-CT scanning using 2-deoxy-2-((18)F)fluoro-D-glucose. Interestingly, after 24 hours reperfusion diabetic mice showed a reduced infarct size and less apoptosis indicated by TUNEL analysis in heart sections. This may be explained by increased levels of autophagy detected in diabetic mice hearts. Similar increases in IR-induced macrophage infiltration detected by CD68 staining indicated no change in inflammation between control and diabetic mice. Over time, control mice subjected to IR developed mild left ventricular dilation whereas diabetic mice exhibited a decrease in both end diastolic left ventricular volume and LVESV with a decreased intraventricular space and thicker left ventricular wall, indicating concentric hypertrophy. This was associated with marked increases in fibrosis, indicted by Masson trichrome staining, of heart sections in diabetic IR group. In summary, we demonstrate that diabetes principally influences distinct IR-induced chronic changes in cardiac function and remodeling, while a smaller infarct size and elevated levels of autophagy with similar cardiac function are observed in acute phase.Megumi EguchiYoung Hwa KimKeon Wook KangChi Young ShimYangsoo JangThierry DorvalKwang Joon KimGary SweeneyPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 2, p e30450 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Megumi Eguchi
Young Hwa Kim
Keon Wook Kang
Chi Young Shim
Yangsoo Jang
Thierry Dorval
Kwang Joon Kim
Gary Sweeney
Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
description Diabetes is associated with higher incidence of myocardial infarction (MI) and increased propensity for subsequent events post-MI. Here we conducted a temporal analysis of the influence of diabetes on cardiac dysfunction and remodeling after ischemia reperfusion (IR) injury in mice. Diabetes was induced using streptozotocin and IR performed by ligating the left anterior descending coronary artery for 30 min followed by reperfusion for up to 42 days. We first evaluated changes in cardiac function using echocardiography after 24 hours reperfusion and observed IR injury significantly decreased the systolic function, such as ejection fraction, fractional shortening and end systolic left ventricular volume (LVESV) in both control and diabetic mice. The longitudinal systolic and diastolic strain rate were altered after IR, but there were no significant differences between diabetic mice and controls. However, a reduced ability to metabolize glucose was observed in the diabetic animals as determined by PET-CT scanning using 2-deoxy-2-((18)F)fluoro-D-glucose. Interestingly, after 24 hours reperfusion diabetic mice showed a reduced infarct size and less apoptosis indicated by TUNEL analysis in heart sections. This may be explained by increased levels of autophagy detected in diabetic mice hearts. Similar increases in IR-induced macrophage infiltration detected by CD68 staining indicated no change in inflammation between control and diabetic mice. Over time, control mice subjected to IR developed mild left ventricular dilation whereas diabetic mice exhibited a decrease in both end diastolic left ventricular volume and LVESV with a decreased intraventricular space and thicker left ventricular wall, indicating concentric hypertrophy. This was associated with marked increases in fibrosis, indicted by Masson trichrome staining, of heart sections in diabetic IR group. In summary, we demonstrate that diabetes principally influences distinct IR-induced chronic changes in cardiac function and remodeling, while a smaller infarct size and elevated levels of autophagy with similar cardiac function are observed in acute phase.
format article
author Megumi Eguchi
Young Hwa Kim
Keon Wook Kang
Chi Young Shim
Yangsoo Jang
Thierry Dorval
Kwang Joon Kim
Gary Sweeney
author_facet Megumi Eguchi
Young Hwa Kim
Keon Wook Kang
Chi Young Shim
Yangsoo Jang
Thierry Dorval
Kwang Joon Kim
Gary Sweeney
author_sort Megumi Eguchi
title Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
title_short Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
title_full Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
title_fullStr Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
title_full_unstemmed Ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
title_sort ischemia-reperfusion injury leads to distinct temporal cardiac remodeling in normal versus diabetic mice.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/f90ba337ddc349d187ea71a2d58db1b0
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AT keonwookkang ischemiareperfusioninjuryleadstodistincttemporalcardiacremodelinginnormalversusdiabeticmice
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