Publications (2)1.39 Total impact
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ABSTRACT: 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 1day. Further validation of this hypothesis will provide additional insight of the molecular mechanism of myocardium maturation.Medical Hypotheses 05/2012; 79(2):174-7. · 1.39 Impact Factor
Article: [Expression of bone morphogenetic protein receptor 2 in myocardialization of cardiac proximal outflow tract septum in connexin 43 knockout embryonic mice].[show abstract] [hide abstract]
ABSTRACT: To investigate the mechanism of myocardialization of proximal outflow tract septum and its effect on the conotruncal anomaly in mice. The C(57)/BL(6) mice of embryonic day (E) 11.5 - 16.5 were selected. The phenotypes of connexin 43 (Cx43) homozygotes (Cx43(-/-)), heterozygotes (Cx43(+/-)) and wild-types (Cx43(+/+)) were genetically typed by polymerase chain reaction (PCR). Bone morphogenetic protein receptor 2 (Bmpr2) and α-sarcomeric acti (α-SCA) were detected by immunohistochemistry. The expression of α-SCA in the proximal outflow tract (OFT) septum was delayed obviously in Cx43(-/-) predominantly at E13.5 and E14.5. From E11.5 to E13.5, the expression of Bmpr2 was detected in cardiac atrium and epicardium of Cx43(+/+) fetal heart. And Bmpr2 was slightly expressed in ventricular muscle of Cx43(+/+) fetal heart. And it was expressed slightly only in cardiac atrium and epicardium of Cx43(+/-) and Cx43(-/-) fetal heart. From E14.5 to E16.5, its expression was detected obviously in cardiac atrium, epicardium, endocardium, trabeculum, ventricular muscle and OFT septum of Cx43(+/+) fetal heart. At E14.5, its expression was detected obviously in cardiac atrium, epicardium, endocardium and trabeculum of Cx43(+/-) and Cx43(-/-) fetal heart while none in ventricular muscle and OFT septum. At E15.5 and E16.5, its expression was detected obviously in cardiac atrium, epicardium, endocardium, trabeculum, ventricular muscle and OFT septum of Cx43(+/-) and Cx43(-/-) fetal heart. Its expression was also detected obviously in OFT septum of Cx43(+/-) and Cx43(-/-) fetal heart with incomplete myocardialization. Cx43KO embryonic mice exhibit delayed myocardialization. As compared with the Cx43(+/+), the expression of Bmpr2 in proximal OFT septum was delayed obviously in Cx43(+/-) and Cx43(-/-) mice. And the expression of Bmpr2 is abnormal in OFT septum of Cx43(+/-) and Cx43(-/-) fetal heart. Bmpr2 may be involved in the interaction between epicardium and myocardium. It may be a critical mechanism in the maturation process of cardiac muscles.Zhonghua yi xue za zhi 08/2011; 91(31):2211-5.