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Determination of cell types and numbers during cardiac development in the neonatal and adult rat and mouse

心肌细胞 心室 胶原酶 生物 心室 心脏发育 细胞 电池类型 心肌 单元格排序 内科学 细胞生物学 内分泌学 胚胎干细胞 男科 医学 遗传学 基因 生物化学
作者
Indroneal Banerjee,John W. Fuseler,Robert L. Price,Thomas K. Borg,Troy A. Baudino
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology [American Physiological Society]
卷期号:293 (3): H1883-H1891 被引量:619
标识
DOI:10.1152/ajpheart.00514.2007
摘要

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 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 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 ∼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 numbers of cardiac fibroblasts and a resultant decrease in percentages 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 enabled us to establish a homeostatic model for the myocardium that can be compared with genetic and cardiac disease models.
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