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Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury
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Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury
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Journal Article
Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury
2018
Overview
Background
Histone deacetylases (HDACs) play a critical role in modulating myocardial protection and cardiomyocyte survivals. However, Specific HDAC isoforms in mediating myocardial ischemia/reperfusion injury remain currently unknown.
We used cardiomyocyte-specific overexpression of active HDAC4 to determine the functional role of activated HDAC4 in regulating myocardial ischemia and reperfusion in isovolumetric perfused hearts.
Methods
In this study, we created myocyte-specific active HDAC4 transgenic mice to examine the functional role of active HDAC4 in mediating myocardial I/R injury. Ventricular function was determined in the isovolumetric heart, and infarct size was determined using tetrazolium chloride staining.
Results
Myocyte-specific overexpressing activated HDAC4 in mice promoted myocardial I/R injury, as indicated by the increases in infarct size and reduction of ventricular functional recovery following I/R injury. Notably, active HDAC4 overexpression led to an increase in LC-3 and active caspase 3 and decrease in SOD-1 in myocardium. Delivery of chemical HDAC inhibitor attenuated the detrimental effects of active HDAC4 on I/R injury, revealing the pivotal role of active HDAC4 in response to myocardial I/R injury.
Conclusions
Taken together, these findings are the first to define that activated HDAC4 as a crucial regulator for myocardial ischemia and reperfusion injury.
Publisher
BioMed Central,Springer Nature B.V,BMC
Subject
/ Biomedical and Life Sciences
/ Heart
/ Histone Deacetylase Inhibitors - pharmacology
/ Histone deacetylase4 (HDAC4)
/ Histone Deacetylases - genetics
/ Histone Deacetylases - metabolism
/ Ischemia
/ Male
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - physiopathology
/ Myocardial Reperfusion Injury - metabolism
/ Myocardial Reperfusion Injury - physiopathology
/ Myocytes, Cardiac - metabolism
/ Myocytes, Cardiac - physiology
/ Proteins
/ Swine
