cardiovascular system
• at 1 month after myocardial infarction, mice exhibit a lower ejection fraction and fractional shortening of the left ventricle than wild-type controls
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• at 1 month, but not at 1 week, after myocardial infarction, mice exhibit higher cardiac fibrosis levels than wild-type controls and cardiac tissue is more fragile with ~90% of the heart sections exhibiting breakage in the injured area relative to ~10% in sections from wild-type hearts
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cellular
• when cultured in vitro under differentiating conditions, c-Kit+ cardiac progenitor cells (CPCs) isolated from homozygous mutant mice show reduced expression of both early and late cardiomyocyte markers
• at 1 week after myocardial infarction, mice fail to show an increase in the percentage of double-positive (c-Kit+/Gata4+) cells suggesting that CPC differentiation/commitment is inhibited, unlike in wild-type controls
• however, cardiomyocyte proliferation in the border zone is normal at 1 week after myocardial injury
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• in vitro, c-Kit+ CPCs isolated from homozygous mutant mice exhibit a higher proliferative capacity than wild-type cells
• in vivo, c-Kit+ CPC number and proliferative capacity are increased
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homeostasis/metabolism
• at 1 month, but not at 1 week, after myocardial infarction, mice exhibit higher cardiac fibrosis levels than wild-type controls and cardiac tissue is more fragile with ~90% of the heart sections exhibiting breakage in the injured area relative to ~10% in sections from wild-type hearts
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muscle
• at 1 month after myocardial infarction, mice exhibit a lower ejection fraction and fractional shortening of the left ventricle than wild-type controls
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