Key result
Protein disulfide isomerase gene transfer yields ~2.5-fold smaller infarcts and reduces apoptosis in MI mice.
Why the study?
The molecular mechanisms of initial response to ischemic insult in the heart and pathways involved in compensation and remodeling are still largely unknown.
Population
Human viable peri-infarct myocardial tissue and HL1 cardiomyocyte cells; mouse model of myocardial infarction
Comparison
Up-regulation vs down-regulation of gene expression; PDI gene transfer vs transgene-null vector
Design
Gene expression analysis, in vitro hypoxia model, and in vivo mouse myocardial infarction model
Authors
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Laboratory study demonstrates that protein disulfide isomerase promotes cardiomyocyte survival during ischemic injury, suggesting a novel therapeutic target for heart failure.
Severino et al. (2007) studied Ischemic Cardiomyopathy. Adenoviral-mediated Protein Disulfide Isomerase (PDI) gene transfer vs. Transgene-null adenoviral vector was evaluated on Infarct size, cardiomyocyte apoptosis, and left ventricular end-diastolic diameter. Adenoviral-mediated Protein Disulfide Isomerase gene transfer in a mouse model of myocardial infarction resulted in a 2.5-fold smaller infarct size and significantly reduced apoptosis.
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