Sonic hedgehog is required for cardiac outflow tract and neural crest cell development
Sonic hedgehog is required for cardiac outflow tract and neural crest cell development
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DOI：
10.1016/j.ydbio.2005.04.029
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发表时间：
2005-07-15
影响因子：
2.7
通讯作者：
Meyers, EN
中科院分区：
文献类型：
--
作者：
Smoak, IW;Byrd, NA;Meyers, EN
Hedgehog信号通路对许多发育模式事件至关重要。在这项研究中，我们重点研究了Sonic hedgehog(Shh)缺失小鼠胚胎中存在的咽弓和心血管图案的缺陷。我们的数据表明，在没有Shh的情况下，咽弓发育普遍失败，导致心脏和颅面部缺陷。心脏表型由弓状动脉和流出道构型缺陷以及移行神经脊细胞(NCC)的异常发育所致。心血管缺陷的星座类似于人类出生缺陷综合征法洛四联症的一种严重形式，并伴有完全性肺动脉闭锁。先前的研究已经证明Shh在NCC发育后期的存活和增殖中起作用。我们的数据表明，SHH信号并不直接作用于NCC作为生存因子，而是在心血管和颅面发育的早期阶段(e8.5-10.5)限制NCC可以填充的区域。(C)2005 Elsevier Inc.保留所有权利。
The Hedgehog signaling pathway is critical for a significant number of developmental patterning events. In this study, we focus on the defects in pharyngeal arch and cardiovascular patterning present in Sonic hedgehog (Shh) null mouse embryos. Our data indicate that, in the absence of Shh, there is general failure of the pharyngeal arch development leading to cardiac and craniofacial defects. The cardiac phenotype results from arch artery and outflow tract patterning defects, as well as abnormal development of migratory neural crest cells (NCCs). The constellation of cardiovascular defects resembles a severe form of the human birth defect syndrome tetralogy of Fallot with complete pulmonary artery atresia. Previous studies have demonstrated a role for Shh in NCC survival and proliferation at later stages of development. Our data suggest that SHH signaling does not act directly on NCCs as a survival factor, but rather acts to restrict the domains that NCCs can populate during early stages (e8.5 - 10.5) of cardiovascular and craniofacial development. (c) 2005 Elsevier Inc. All rights reserved.