Journal
HEART
Volume 95, Issue 14, Pages 1159-1164Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/hrt.2008.150128
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Funding
- Hein J J Wellens Foundation
- Foundation De Drie Lichten
- Heart Lung and Blood Institutes of the National Institutes of Health (USA)
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Background: Transgenic mice expressing the dominant interfering p193 protein in cardiomyocytes (MHC-1152stop mice) exhibit an induction of cell cycle activity and altered remodelling after experimental myocardial infarction (MI). Objective: To determine whether the altered remodelling results in improved cardiac function in the MHC-1152stop mice after MI, as compared with non-transgenic mice. Methods: MHC-1152stop mice and non-transgenic littermates were subjected to experimental MI via permanent occlusion of the coronary artery. Infarct size was determined at 24 h and at 4 weeks after MI, and left ventricular pressure-volume measurements were performed at 4 weeks after MI in infarcted and sham-operated animals. Results: Infarct size in MHC-1152stop mice and non-transgenic littermates was not statistically different at 24 h after MI, as measured by tetrazolium staining. Morphometric analysis showed that infarct scar expansion at 4 weeks after MI was reduced by 10% in the MHC-1152stop mice (p < 0.05). No differences in cardiac function were detected between sham-operated MHC-1152stop mice and their non-transgenic littermates. However, at 4 weeks after MI, the ventricular isovolumic relaxation time constant (tau) was decreased by 19% (p < 0.05), and the slope of the dP/dt(max)-EDV relationship was increased 99% (p < 0.05), in infarcted MHC-1152 stop mice as compared with infarcted non-transgenic littermates. Conclusion: Expression of the dominant interfering p193 transgene results in a decrease in infarct scar expansion and preservation of myocardial function at 4 weeks after MI. Antagonism of p193 activity may represent an important strategy for the treatment of MI.
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