Survey of Studies Examining Mammalian Cardiomyocyte DNA Synthesis

From the Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis.

Correspondence to Dr Loren J. Field, Krannert Institute of Cardiology, 1111 West 10th St, Indianapolis, IN 46202-4800. E-mail FIELD@KIMAIL.DMED.IUPUI.EDU

Key Words: DNA synthesis • cardiomyocyte • development

	Introduction

 
Increases in cardiac mass during fetal life arise predominantly as a consequence of cardiomyocyte proliferation. During neonatal life, there is a transition from hyperplastic to hypertrophic growth such that further increases in myocardial mass are typically not accompanied by cardiomyocyte proliferation. In the adult myocardium, it is generally believed that the vast majority of cardiomyocytes do not proliferate. This view is supported in part by clinical observations: functionally significant myocardial regeneration has not been documented in diseases and/or injuries that result in cardiomyocyte loss. Furthermore, primary myocardial tumors are rarely observed in adults.

Although these findings suggest that the proliferative capacity of adult cardiomyocytes is quite low, they do not exclude the existence of a limited degree of hyperplastic growth in either the normal or diseased myocardium. Toward this end, a number of studies examining the proliferative capacity of cardiomyocytes in experimental animals have been reported. Because genome reduplication is a prerequisite for cell proliferation, the majority of these studies have used various methodologies to monitor cardiomyocyte DNA synthesis as a first approximation of cell division. In the present survey, issues that we consider pertinent for accurate assessment of cardiomyocyte DNA synthesis are discussed. The literature examining cardiomyocyte DNA synthesis during normal and pathological myocardial growth is then summarized.

	Assessment of Cardiomyocyte DNA Synthesis In Vivo

 
Accurate assessment of cardiomyocyte DNA synthesis in vivo is dependent on the selection of an appropriate marker for genome reduplication as well as the criteria used for cardiomyocyte identification. These issues are considered separately below.

Markers for DNA Synthesis
Genome reduplication is accompanied by a . . . [Full Text of this Article]

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				J.-M. Li and G. Brooks Cell cycle regulatory molecules (cyclins, cyclin-dependent kinases and cyclin-dependent kinase inhibitors) and the cardiovascular system; potential targets for therapy? Eur. Heart J., March 2, 1999; 20(6): 406 - 420. [PDF]

				L. M. Pabon-Pena, R. L. Goodwin, L. J. Cise, and D. Bader Analysis of CMF1 Reveals a Bone Morphogenetic Protein-independent Component of the Cardiomyogenic Pathway J. Biol. Chem., July 7, 2000; 275(28): 21453 - 21459. [Abstract] [Full Text] [PDF]

				A. Leri, L. Barlucchi, F. Limana, A. Deptala, Z. Darzynkiewicz, T. H. Hintze, J. Kajstura, B. Nadal-Ginard, and P. Anversa Telomerase expression and activity are coupled with myocyte proliferation and preservation of telomeric length in the failing heart PNAS, July 17, 2001; 98(15): 8626 - 8631. [Abstract] [Full Text] [PDF]

				K. B. S. Pasumarthi, S.-C. Tsai, and L. J. Field Coexpression of Mutant p53 and p193 Renders Embryonic Stem Cell-Derived Cardiomyocytes Responsive to the Growth-Promoting Activities of Adenoviral E1A Circ. Res., May 25, 2001; 88(10): 1004 - 1011. [Abstract] [Full Text] [PDF]

				M. A. Laflamme, D. Myerson, J. E. Saffitz, and C. E. Murry Evidence for Cardiomyocyte Repopulation by Extracardiac Progenitors in Transplanted Human Hearts Circ. Res., April 5, 2002; 90(6): 634 - 640. [Abstract] [Full Text] [PDF]