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1 Cell Developmental Biology and Anatomy, University of South Carolina, Columbia, South Carolina, United States
2 Cell and Developmental Biology and Anatomy, University of South Carolina, Columbia, South Carolina, United States
3 Univ South Carolina; Cell and Developmental Biology and Anatomy, University of South Carolina, Columiba, South Carolina, United States
4 Cell Developmental Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, United States; Columbia, South Carolina, United States
* To whom correspondence should be addressed. E-mail: tbaudino{at}gw.med.sc.edu.
Cardiac fibroblasts, myocytes, endothelial cells and vascular smooth muscle cells are the major cellular constituents of the heart. The aim of this study was to observe alterations in the myocardial cell populations during early neonatal development, in the adult animal and to observe any variations of the cardiac cell populations in different species, specifically the rat and the mouse. Whole hearts were isolated from either mice or rats during the neonatal and adult stages of development and single cell suspensions were prepared via sequential collagenase digestion. Heterogeneous cell populations were immunolabeled for specific cell types and analyzed using Fluorescence Activated Cell Sorting (FACS). In addition, the left ventricle, right ventricle and septa were isolated, fixed and sectioned for morphometric analyses. These same cardiac regions were also analyzed using FACS. We observed that the adult murine myocardium is composed of approximately 56% myocytes, 27% fibroblasts, 7% endothelial cells and 10% vascular smooth muscle cells. Moreover, our morphometric and FACS data demonstrated similar percentages in the three regions examined. During murine neonatal cardiac development, we observed a marked increase in the number of cardiac fibroblasts and a resultant decrease the in the percentage of myocytes in late neonatal development (day 15). Finally, FACS analyses of the rat heart during development displayed similar results in relation to increases in cardiac fibroblasts during development; however, cell populations in the rat differed markedly from those observed in the mouse. Taken together, these data have enabled us to establish a homeostatic model for the myocardium that can be compared to genetic and cardiac disease models.
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