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First published online 31 October 2006
doi: 10.1242/jcs.03252

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Re-programming of newt cardiomyocytes is induced by tissue regeneration

¹ Institute of Physiological Chemistry, Martin-Luther-University Halle-Wittenberg, Hollystrasse 1, 06097 Halle, Germany
² Max-Planck-Institute for Heart and Lung Research, Department of Cardiac Development and Remodelling, Parkstrasse 1, 61231 Bad Nauheim, Germany

^* Author for correspondence (e-mail: thomas.braun{at}kerckhoff.mpg.de)

Accepted 7 September 2006

Newt hearts are able to repair substantial cardiac injuries without functional impairment, whereas mammalian hearts cannot regenerate. The cellular and molecular mechanisms that control the regenerative capacity of the newt heart are unknown. Here, we show that the ability of newt cardiomyocytes to regenerate cardiac injuries correlates with their ability to transdifferentiate into different cell types. Mechanical injury of the heart led to a severe reduction of sarcomeric proteins in the myocardium, indicating a partial de-differentiation of adult newt cardiomyocytes during regeneration. Newt cardiomyocytes implanted into regenerating limbs lost their cardiac phenotype and acquired skeletal muscle or chondrocyte fates. Reprogramming of cardiomyocytes depended on contact with the limb blastema because cardiomyocytes implanted into intact, non-regenerating limbs or cultured in vitro retained their original identity. We reason that signals from the limb blastema led to de-differentiation of cardiomyocytes, cell proliferation and re-differentiation into specialized cells and propose that the ability of cardiomyocytes to transdifferentiate into different cell types reflects the cellular program that enables heart regeneration.

Key words: Heart regeneration, Cardiomyocyte, Differentiation, Limb blastema

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