Abnormal venous and arterial patterning in chordin mutants
Abnormal venous and arterial patterning in chordin mutants
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DOI：
10.1002/dvdy.21287
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发表时间：
2007-09-01
影响因子：
2.5
通讯作者：
Bachiller, Daniel
中科院分区：
文献类型：
--
作者：
Delot, Emmanuele C.;Shneyder, Natalya;Bachiller, Daniel
经典的染料注射方法产生了心血管系统正常和病理发展的令人惊讶的详细图像。然而，由于这些方法依赖于心脏跳动的扩散染料，可视化的血管一直局限于动脉树，我们对静脉发育的知识是滞后的。为了解决这个问题，我们将着色的水杨酸甲酯树脂固定并透明后注射到小鼠胚胎中。这项新技术使我们能够对静脉系统进行成像，并促使我们在Chord(-/-)突变小鼠中发现了多种静脉异常。骨形态发生蛋白信号通路的抑制物Chordin的遗传失活会导致神经脊缺陷影响心脏和颈部器官，如DiGeorge综合征患者所见。降主动脉内注射CHRD(-/-)突变体，显示了非常严重的早期主动脉弓表型如何发展成永久性动脉干。此外，注入心房还显示了前主干静脉及其分支的几个图案性缺陷，包括节段缺失、环状和中线缺陷。控制个体头静脉发育的信号尚不清楚，但我们的结果表明，骨形态发生蛋白通路在这一过程中是必要的。
Classic dye injection methods yielded amazingly detailed images of normal and pathological development of the cardiovascular system. However, because these methods rely on the beating heart of diffuse the dyes, the vessels visualized have been limited to the arterial tree, and our knowledge of vein development is lagging. In order to solve this problem, we injected pigmented methylsalicylate resins in mouse embryos after they were fixed and made transparent. This new technique allowed us to image the venous system and prompted the discovery of multiple venous anomalies in Chord(-/-) mutant mice. Genetic inactivation of Chordin, an inhibitor of the Bone Morphogenetic Protein signaling pathway, results in neural crest defects affecting heart and neck organs, as seen in DiGeorge syndrome patients. Injection into the descending aorta of Chrd(-/-) mutants demonstrated how a very severe early phenotype of the aortic arches develops into persistent truncus arteriosus. In addition, injection into the atrium revealed several patterning defects of the anterior cardinal veins and their tributaries, including absence of segments, looping and midline defects. The signals that govern the development of the individual cephalic veins are unknown, but our results show that the Bone Morphogenetic Protein pathway is necessary for the process.