scholarly journals SWI/SNF in cardiac progenitor cell differentiation

2013 ◽  
Vol 114 (11) ◽  
pp. 2437-2445 ◽  
Author(s):  
Ienglam Lei ◽  
Liu Liu ◽  
Mai Har Sham ◽  
Zhong Wang
Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2192
Author(s):  
Lianjie Miao ◽  
Yangyang Lu ◽  
Anika Nusrat ◽  
Hala Y. Abdelnasser ◽  
Sayantap Datta ◽  
...  

Numb family proteins (NFPs), including Numb and Numblike (Numbl), are commonly known for their role as cell fate determinants for multiple types of progenitor cells, mainly due to their function as Notch inhibitors. Previous studies have shown that myocardial NFP double knockout (MDKO) hearts display an up-regulated Notch activation and various defects in cardiac progenitor cell differentiation and cardiac morphogenesis. Whether enhanced Notch activation causes these defects in MDKO is not fully clear. To answer the question, we examined the spatiotemporal patterns of Notch1 expression, Notch activation, and Numb expression in the murine embryonic hearts using multiple approaches including RNAScope, and Numb and Notch reporter mouse lines. To further interrogate the interaction between NFPs and Notch signaling activation, we deleted both Notch1 or RBPJk alleles in the MDKO. We examined and compared the phenotypes of Notch1 knockout, NFPs double knockout, Notch1; Numb; Numbl and RBPJk; Numb; Numbl triple knockouts. Our study showed that Notch1 is expressed and activated in the myocardium at several stages, and Numb is enriched in the epicardium and did not show the asymmetric distribution in the myocardium. Cardiac-specific Notch1 deletion causes multiple structural defects and embryonic lethality. Notch1 or RBPJk deletion in MDKO did not rescue the structural defects in the MDKO but partially rescued the defects of cardiac progenitor cell differentiation, cardiomyocyte proliferation, and trabecular morphogenesis. Our study concludes that NFPs regulate progenitor cell differentiation, cardiomyocyte proliferation, and trabecular morphogenesis partially through Notch1 and play more roles than inhibiting Notch1 signaling during cardiac morphogenesis.


2018 ◽  
Vol 25 (4) ◽  
pp. 809-822 ◽  
Author(s):  
Diego Herrero ◽  
María Tomé ◽  
Susana Cañón ◽  
Francisco M. Cruz ◽  
Rosa María Carmona ◽  
...  

2015 ◽  
Vol 6 (2) ◽  
pp. 137-148 ◽  
Author(s):  
Mingfu Wu ◽  
Jingjing Li

AbstractVertebrate heart formation is a spatiotemporally regulated morphogenic process that initiates with bilaterally symmetric cardiac primordial cells migrating toward the midline to form a linear heart tube. The heart tube then elongates and undergoes a series of looping morphogenesis, followed by expansions of regions that are destined to become primitive heart chambers. During the cardiac morphogenesis, cells derived from the first heart field contribute to the primary heart tube, and cells from the secondary heart field, cardiac neural crest, and pro-epicardial organ are added to the heart tube in a precise spatiotemporal manner. The coordinated addition of these cells and the accompanying endocardial cushion morphogenesis yield the atrial, ventricular, and valvular septa, resulting in the formation of a four-chambered heart. Perturbation of progenitor cells’ deployment and differentiation leads to a spectrum of congenital heart diseases. Two of the genes that were recently discovered to be involved in cardiac morphogenesis are Numb and Numblike. Numb, an intracellular adaptor protein, distinguishes sibling cell fates by its asymmetric distribution between the two daughter cells and its ability to inhibit Notch signaling. Numb regulates cardiac progenitor cell differentiation in Drosophila and controls heart tube laterality in Zebrafish. In mice, Numb and Numblike, the Numb family proteins (NFPs), function redundantly and have been shown to be essential for epicardial development, cardiac progenitor cell differentiation, outflow tract alignment, atrioventricular septum morphogenesis, myocardial trabeculation, and compaction. In this review, we will summarize the functions of NFPs in cardiac development and discuss potential mechanisms of NFPs in the regulation of cardiac development.


Autophagy ◽  
2019 ◽  
Vol 15 (7) ◽  
pp. 1182-1198 ◽  
Author(s):  
Mark A. Lampert ◽  
Amabel M. Orogo ◽  
Rita H. Najor ◽  
Babette C. Hammerling ◽  
Leonardo J. Leon ◽  
...  

2010 ◽  
Vol 23 (4) ◽  
pp. 514-518 ◽  
Author(s):  
Stefania Pagliari ◽  
Ana Cristina Vilela-Silva ◽  
Giancarlo Forte ◽  
Francesca Pagliari ◽  
Corrado Mandoli ◽  
...  

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