Abstract
It has been generally believed that cardiomyocytes (CMs) are terminally differentiated cells and have little ability to proliferate. Consequently, acutely injured hearts do not regenerate, and develop fibrosis and scarring. It has been previously reported that the mammalian heart induces CMs- proliferation after injury but the rate of proliferation is too low to repair the heart. In addition, recent studies have shown that co-treatment of CMs with FGF1 and p38 MAPK inhibitor (p38i) induces proliferation of cardiomyocytes. However, the detailed mechanisms for the proliferation ability of CMs have not been fully understood. In this study, we have tried to characterize changes in the proliferation ability by co-treatment with FGF1 and p38i. In addition, we also performed immunocytochemical and Western blot analyses to identify the expression and distribution of connexin 43, a primary gap junction protein in CMs. Finally, we examined changes in the spontaneous beating of CMs by co-treatment with FGF1 and p38i. The present findings are expected to develop novel approaches for the regeneration of the heart after injury. [J Physiol Sci. 2008;58 Suppl:S184]
