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Abstract：
Proper development of the great vessels of the heart and septation of the cardiac outflow tract requires cardiac neural crest cells. These cells give rise to the parasympathetic cardiac ganglia, the smooth muscle layer of the great vessels, some cardiomyocytes, and the conotruncal cushions and aorticopulmonary septum of the outflow tract. Ablation of cardiac neural crest cells results in defective patterning of each of these structures. Previous studies have shown that targeted deletion of the forkhead transcription factor C2 (Foxc2), results in cardiac phenotypes similar to that derived from cardiac neural crest cell ablation.
We report that Foxc2-/- embryos on the 129s6/SvEv inbred genetic background display persistent truncus arteriosus and hypoplastic ventricles before embryonic lethality. Foxc2 loss-of-function resulted in perturbed cardiac neural crest cell migration and their reduced contribution to the outflow tract as evidenced by lineage tracing analyses together with perturbed expression of the neural crest cell markers Sox10 and Crabp1. Foxc2 loss-of-function also resulted in alterations in PlexinD1, Twist1, PECAM1, and Hand1/2 expression in association with vascular and ventricular defects.
Our data indicate Foxc2 is required for proper migration of cardiac neural crest cells, septation of the outflow tract, and development of the ventricles. Developmental Dynamics 247:1286-1296, 2018. © 2018 Wiley Periodicals, Inc.
We report that Foxc2-/- embryos on the 129s6/SvEv inbred genetic background display persistent truncus arteriosus and hypoplastic ventricles before embryonic lethality. Foxc2 loss-of-function resulted in perturbed cardiac neural crest cell migration and their reduced contribution to the outflow tract as evidenced by lineage tracing analyses together with perturbed expression of the neural crest cell markers Sox10 and Crabp1. Foxc2 loss-of-function also resulted in alterations in PlexinD1, Twist1, PECAM1, and Hand1/2 expression in association with vascular and ventricular defects.
Our data indicate Foxc2 is required for proper migration of cardiac neural crest cells, septation of the outflow tract, and development of the ventricles. Developmental Dynamics 247:1286-1296, 2018. © 2018 Wiley Periodicals, Inc.
摘要：
心脏大血管的适当发育和心脏流出道的分隔需要心脏神经c细胞。这些细胞产生副交感神经心神经节，大血管的平滑肌层，一些心肌细胞，以及流出道的锥形垫和主肺隔膜。心脏神经c细胞的消融导致这些结构中的每一个的有缺陷的图案形成。先前的研究表明，叉头转录因子C2（Foxc2）的靶向缺失，结果心脏表型与心脏神经c细胞消融相似。
我们报告说，129s6/SvEv近交遗传背景上的Foxc2-/-胚胎在胚胎致死之前表现出持续的动脉干和发育不良的心室。Foxc2功能丧失导致心脏神经c细胞迁移受到干扰，并且它们对流出道的贡献减少，如谱系追踪分析以及神经c细胞标记物Sox10和Crabp1的表达受到干扰所证明。Foxc2功能丧失还导致与血管和心室缺陷相关的PlexinD1、Twist1、PECAM1和Hand1/2表达的改变。
我们的数据表明Foxc2是心脏神经c细胞正常迁移所必需的，流出道的分隔，和心室的发育。发展动态247：1286-1296，2018。©2018Wiley期刊，Inc.
我们报告说，129s6/SvEv近交遗传背景上的Foxc2-/-胚胎在胚胎致死之前表现出持续的动脉干和发育不良的心室。Foxc2功能丧失导致心脏神经c细胞迁移受到干扰，并且它们对流出道的贡献减少，如谱系追踪分析以及神经c细胞标记物Sox10和Crabp1的表达受到干扰所证明。Foxc2功能丧失还导致与血管和心室缺陷相关的PlexinD1、Twist1、PECAM1和Hand1/2表达的改变。
我们的数据表明Foxc2是心脏神经c细胞正常迁移所必需的，流出道的分隔，和心室的发育。发展动态247：1286-1296，2018。©2018Wiley期刊，Inc.
