Cadherin2 (N-cadherin) plays an essential role in zebrafish cardiovascular development.
Cadherin2 (N-cadherin) plays an essential role in zebrafish cardiovascular development.
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DOI：
10.1186/1471-213x-6-23
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发表时间：
2006-05-23
影响因子：
--
通讯作者：
Liu Q
中科院分区：
文献类型：
--
作者：
Bagatto B;Francl J;Liu B;Liu Q
钙粘蛋白是细胞表面粘附分子，在脊椎动物组织和器官的发育中发挥重要作用。我们利用原位杂交和免疫细胞化学方法研究了发育中的斑马鱼心脏中钙粘蛋白2的表达，发现胚胎斑马鱼的心肌强烈表达钙粘蛋白2。为了深入了解钙粘蛋白2在心脏形成和功能中的作用，我们分析了钙粘蛋白2突变体玻璃洋葱（glo）的心脏分化和性能。我们发现钙粘蛋白2突变体心包腔扩大，心房和心室紊乱，心室特异性标记物vmhc的表达减少。 glo 突变体胚胎中的单个心肌细胞变成圆形并松散聚集。心脏性能的体内测量表明，与对照胚胎相比，突变心脏的心率、每搏输出量和心输出量显着降低。 glo 突变体中胚胎血管系统的形成也受到影响。我们的结果表明钙粘蛋白2在斑马鱼心血管发育中发挥重要作用。尽管心包扩大和外周血流量减少的确切机制尚不清楚，但很明显，当钙粘蛋白2功能受到破坏时，心肌细胞分化和生理心血管功能会受到损害。
Cadherins are cell surface adhesion molecules that play important roles in development of vertebrate tissues and organs. We studied cadherin2 expression in developing zebrafish heart using in situ hybridization and immunocytochemical methods, and we found that cadherin2 was strongly expressed by the myocardium of the embryonic zebrafish. To gain insight into cadherin2 role in the formation and function of the heart, we analyzed cardiac differentiation and performance in a cadherin2 mutant, glass onion (glo). We found that the cadherin2 mutant had enlarged pericardial cavity, disorganized atrium and ventricle, and reduced expression of a ventricular specific marker vmhc. Individual myocardiocytes in the glo mutant embryos became round shaped and loosely aggregated. In vivo measurements of cardiac performance revealed that the mutant heart had significantly reduced heart rate, stroke volume and cardiac output compared to control embryos. Formation of the embryonic vascular system in the glo mutants was also affected. Our results suggest that cadherin2 plays an essential role in zebrafish cardiovascular development. Although the exact mechanisms remain unknown as to the formation of the enlarged pericardium and reduced peripheral blood flow, it is clear that myocardiocyte differentiation and physiological cardiovascular performance is impaired when cadherin2 function is disrupted.