14-3-3epsilon controls multiple developmental processes in the mouse heart

摘要: Background: 14-3-3e plays an important role in the maturation of compact ventricular myocardium by modulating cardiomyocyte cell cycle via p27kip1. However, additional cardiac defects are possible given ubiquitous expression pattern this protein. Results: Germ line deletion 14-3-3e led to malalignment both outflow tract (OFT) and atrioventricular (AV) cushions, with resulting tricuspid stenosis atresia, mitral valve abnormalities, perimembranous septal (VSDs). We confirmed myocardial non-compaction detected a spongy septum muscular VSDs blebbing epicardium. These were associated abnormal patterning p27kip1 subendocardial possibly epicardial populations. In addition pharyngeal arch artery patterning, we found deep endocardial recesses paucity intramyocardial coronary vasculature as result defective plexus remodeling. Conclusions: The cushions provides new explanation for defects, while basis patterning. abnormalities might arise from dysregulation defect epithelial-to-mesenchymal transformation. data suggest that 14-3-3e, left (LVNC), be linked different forms congenital heart disease (CHD). Developmental Dynamics 245:1107–1123, 2016. © 2016 Wiley Periodicals, Inc.