Epicardium-derived cells (EPDCs) can migrate into the myocardium, giving rise to several types of cell which are indispensable to compact myocardium and inducing normal myocardial development. Subepicardium accumulates bone morphogenetic proteins (Bmps), which can release into myocardium further. It has been shown that reduced Bmp-mediated signaling in a novel neural crest derivative in the epicardium reduced the cardiomyocyte proliferative activity in the developing myocardium. Furthermore, studies have demonstrated that cardiomyocytes can develop in proepicardial organ (PEO) explant cultures after stimulation with bone morphogenetic protein (Bmp2). We present a hypothesis that Bmp2 regulates the interaction between EPDCs and cardiomyocyte in the developing outflow tract (OFT). Our previous empirical data also shows that Bmp2 is expressed in the myocardial cell in the OFT at embryonic day (E) 14.5 in wild-type mice, and expression of Bmp2 in Cx43α1 knockout (KO) OFT was delayed for 1. day. Further validation of this hypothesis will provide additional insight of the molecular mechanism of myocardium maturation.
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