Editorials |
From the University Lab of Physiology, Oxford, UK.
Correspondence to Peter Kohl, MD, PhD, University Lab of Physiology, Parks Road, Oxford OX1 3PT, UK. E-mail peter.kohl@physiol.ox.ac.uk
Key Words: cardiomyocytes cardiac fibroblasts gap junctions in vitro in vivo
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The heart is a muscle. Muscles are made up of myocytes. These may differ in form and function, butin essencethey are the cells in which we are interested when we consider the structural makeup of the heart. Likewise, when we assess electrical coupling of cardiac cells by connexins, we are often content to assume that gap junctions occur exclusivelyor at least in the overwhelming majority of casesbetween homologous cell types.
It is sobering, in this context, to reflect on the fact that cardiac myocytes form a minority of cells in the heart, insofar as cell numbers are concerned (which, for cell coupling, is more relevant than total volume occupied by a cell population). A meticulous study by Adler et al1 demonstrated that myocyte and connective tissue cell numbers increase at a similar rate in early human development, from about 0.5x109 at 28 weeks of fetal development to 2 to 3x109 several weeks postpartum. Thereafter, myocyte cell numbers remain stable, while the connective tissue cell count increases with cardiac weight to
7x109 at 2 months of age.
This mitotic potential of cardiac fibroblasts is maintained after cell isolation and is the key reason for which fibroblasts are omnipresent in primary cardiac cell cultures. This is not for lack of effort to eliminate nonmyocytes. Measures to enrich myocyte content in cardiac cell culture include addition of mitotic inhibitors, substrate restrictions, and, most prominently, preplating steps (occasionally in the presence of antibodies against muscle cell surface adhesion
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