Embryonic atrial function is essential for mouse embryogenesis, cardiac morphogenesis and angiogenesis
Embryonic atrial function is essential for mouse embryogenesis, cardiac morphogenesis and angiogenesis
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DOI：
10.1242/dev.00831
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发表时间：
2003-12-01
期刊：
影响因子：
4.6
通讯作者：
Chen, J
中科院分区：
文献类型：
--
作者：
Huang, CQ;Sheikh, F;Chen, J
心脏发育对心房功能的要求尚不清楚。为了解决这个问题，我们培育了心房肌球蛋白轻链 2 (MLC2a) 缺陷的小鼠，心房肌原纤维装置的主要结构组成部分。 Mlc2a 基因失活导致心房收缩严重减弱，并导致 ED10.5-11.5 胚胎死亡，这表明心房功能对于胚胎发生至关重要。我们的数据还解决了心血管发育中两个长期存在的问题：心脏形态发生过程中功能和形式之间的联系，以及血管发育过程中对心脏功能的要求。 MLC2a 缺失胚胎中心房功能的减弱导致心脏形态发生和血管生成方面出现许多一致的继发性异常。我们的结果明确证明，正常的心脏功能与心脏和脉管系统的正常形态发育直接相关。这些数据对先天性心脏病的病因学具有重要意义。
The requirement for atrial function in developing heart is unknown. To address this question, we have generated mice deficient in atrial myosin light chain 2 (MLC2a), a major structural component of the atrial myofibrillar apparatus. Inactivation of the Mlc2a gene resulted in severely diminished atrial contraction and consequent embryonic lethality at ED10.5-11.5, demonstrating that atrial function is essential for embryogenesis. Our data also address two longstanding questions in cardiovascular development: the connection between function and form during cardiac morphogenesis, and the requirement for cardiac function during vascular development. Diminished atrial function in MLC2a-null embryos resulted in a number of consistent secondary abnormalities in both cardiac morphogenesis and angiogenesis. Our results unequivocally demonstrate that normal cardiac function is directly linked to normal morphogenic development of heart and vasculature. These data have important implications for the etiology of congenital heart disease.