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Cardiac Neural Crest (cardiac + neural_crest)
Selected AbstractsCharacterization of molecular markers to assess cardiac cushions formation in XenopusDEVELOPMENTAL DYNAMICS, Issue 12 2009Young-Hoon Lee Abstract The valves and septa of the mature heart are derived from the cardiac cushions, which develop from discrete swellings in two regions of developing heart tube: the atrioventricular (AV) canal and the ventricular outflow tract (OFT). In higher vertebrates, three distinct lineages contribute to the heart valves and septa, the endocardium, the myocardium, and the cardiac neural crest that will populate the cardiac jelly of the OFT. Very little is known about cardiac cushions development in amphibians. Here, we describe the expression of eight genes during key stages of cardiac cushion development in Xenopus. Among these genes, the Wnt antagonist Frzb1 and the transcription factors Xl-Fli, Sox8, Sox9, and Sox10 are differentially expressed in the mesenchyme of the OFT and AV cushions. These genes can be used in combination with lineage-tracing experiments to determine the embryonic origin of the cardiac cushions mesenchyme in Xenopus. Developmental Dynamics 238:3257,3265, 2009. © 2009 Wiley-Liss, Inc. [source] Coordinated and conserved expression of alphoid repeat and alphoid repeat-tagged coding sequencesDEVELOPMENTAL DYNAMICS, Issue 1 2003Yin-Xiong Li Abstract We have found an alpha-like simple-sequence DNA repeat that is differentially expressed during early embryogenesis in both chick and zebrafish. Before and during the primitive streak stage, transcripts of the alphoid repeat sequence were ubiquitously expressed throughout zebrafish and chick embryos. After headfold formation, expression was limited to the cardiac neural crest, the head, and the heart. Two types of alphoid repeat sequence transcripts were identified: alphoid repeat RNA and alphoid repeat-tagged mRNA (ES,T). Several of the ES,Ts were identified by (1) searching expressed sequence tag databases, (2) arbitrary rapid amplification of cDNA ends (RACE), and (3) screening embryonic cDNA libraries. The alphoid element was located in the 3, untranslated region of one ES,T that was obtained by RACE. The ES,T sequences encoded a variety of different types of proteins, but all were expressed within tissues that were positive for the alphoid repeat RNA. The presence of two types of coordinately expressed alphoid-like repeat transcripts in maternal RNA with subsequent restriction to the head and heart, and the conservation of these features in disparate vertebrate embryos, suggest that the alphoid repeat sequence may serve as a control element in the gene regulation network. Developmental Dynamics 228:72,81, 2003. © 2003 Wiley-Liss, Inc. [source] Synthetic matrix metalloproteinase inhibitor decreases early cardiac neural crest migration in chicken embryosDEVELOPMENTAL DYNAMICS, Issue 4 2002D.H. Cai Abstract During early embryonic development, cardiac neural crest (NC) cells emerge from the forming neural tube, migrate beneath the ectoderm, enter the pharyngeal arches, and subsequently participate in the septation of the heart. Like tumor cells, NC cells penetrate through basement membranes and invade extracellular matrix during their emigration and migration and, therefore, are liable to use similar invasive mechanisms. Matrix metalloproteinases (MMPs) are a family of zinc proteolytic enzymes known to be important in cell migration and invasion of normal and metastatic cells. In an earlier study, we found that the spatial and temporal distribution pattern of MMP-2 positively correlates with cardiac NC migration, suggesting MMP enzymatic activity may be important in mediating cardiac cell NC migration. To test this hypothesis, a synthetic MMP inhibitor, KB8301, was used to block MMP enzymatic activity during in vitro and in vivo cardiac NC cell migration in chick embryos. Injection of KB8301 into the cell-free space adjacent to the neural tube at the level of the second somite before the NC cells emigrated caused major morphologic anomalies in embryos and disrupted cardiac NC morphogenesis. Unilateral injection of KB8301 at lower concentrations, significantly decreased cardiac NC migration on the injected side compared with the noninjected side and compared with that of the injected controls. This decrease correlated with a decrease in MMP activity in the embryos and was not attributable to differences in embryo size or rate of embryonic development after injection. KB8301 also significantly decreased the rate of NC cell motility and distance NC cells migrated from explanted neural tubes and increased cell area and perimeter. These data suggest that MMP enzymatic activity is an important mediator of early cardiac NC migration and that perturbation of endogenous MMP activity may lead to NC-related congenital defects. © 2002 Wiley-Liss, Inc. [source] Developmental consequences of abnormal folate transport during murine heart morphogenesis ,BIRTH DEFECTS RESEARCH, Issue 7 2004Louisa S. Tang Abstract BACKGROUND Folic acid is essential for the synthesis of nucleotides and methyl transfer reactions. Folic acid,binding protein one (Folbp1) is the primary mediator of folic acid transport into murine cells. Folbp1 knockout mouse embryos die in utero with multiple malformations, including severe congenital heart defects (CHDs). Although maternal folate supplementation is believed to prevent human conotruncal heart defects, its precise role during cardiac morphogenesis remains unclear. In this study, we examined the role of folic acid on the phenotypic expression of heart defects in Folbp1 mice, mindful of the importance of neural crest cells to the formation of the conotruncus. METHODS To determine if the Folbp1 gene participates in the commitment and differentiation of the cardiomyocytes, relative levels of dead and proliferating precursor cells in the heart were examined by flow cytometry, Western blot, and immunohistostaining. RESULTS Our studies revealed that impaired folic acid transport results in extensive apoptosis-mediated cell death, which concentrated in the interventricular septum and truncus arteriosus, thus being anatomically restricted to the two regions of congenital heart defects. Together with a reduced proliferative capacity of the cardiomyocytes, the limited size of the available precursor cell pool may contribute to the observed cardiac defects. Notably, there is a substantial reduction in Pax-3 expression in the region of the presumptive migrating cardiac neural crest, suggesting that this cell population may be the most severely affected by the massive cell death. CONCLUSIONS Our findings demonstrate for the first time a prominent role of the Folbp1 gene in mediating susceptibility to heart defects. Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source] | ||||||||||