Max Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.
German Centre for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Bad Nauheim, Germany.
Nat Commun. 2024 Sep 17;15(1):8159. doi: 10.1038/s41467-024-52340-3.
Tissues undergo distinct morphogenetic processes to achieve similarly shaped structures. In the heart, cardiomyocytes in both the ventricle and atrium build internal structures for efficient contraction. Ventricular wall formation (trabeculation) is initiated by cardiomyocyte delamination. How cardiomyocytes build the atrial wall is poorly understood. Using longitudinal imaging in zebrafish, we found that at least 25% of the atrial cardiomyocytes elongate along the long axis of the heart. These cell shape changes result in cell intercalation and convergent thickening, leading to the formation of the internal muscle network. We tested factors important for ventricular trabeculation including Nrg/ErbB and Notch signaling and found no evidence for their role in atrial muscle network formation. Instead, our data suggest that atrial cardiomyocyte elongation is regulated by Yap, which has not been implicated in trabeculation. Altogether, these data indicate that distinct cellular and molecular mechanisms build the internal muscle structures in the atrium and ventricle.
组织经历不同的形态发生过程以实现相似形状的结构。在心脏中,心室和心房中的心肌细胞为有效的收缩构建内部结构。心室壁的形成(小梁化)是由心肌细胞分层启动的。心肌细胞如何构建心房壁还不太清楚。通过在斑马鱼中的纵向成像,我们发现至少 25%的心房心肌细胞沿着心脏的长轴伸长。这些细胞形状的变化导致细胞插入和会聚增厚,从而形成内部肌肉网络。我们测试了对心室小梁化很重要的因素,包括 Nrg/ErbB 和 Notch 信号,但没有发现它们在心房肌肉网络形成中的作用的证据。相反,我们的数据表明,心房心肌细胞的伸长受 Yap 调控,而 Yap 并未被牵连到小梁化中。总的来说,这些数据表明,不同的细胞和分子机制构建了心房和心室的内部肌肉结构。