Synergistic regulation of p53 by Mdm2 and Mdm4 is critical in cardiac endocardial cushion morphogenesis during heart development

2012 ◽  
Vol 228 (3) ◽  
pp. 416-428 ◽  
Author(s):  
Qin Zhang ◽  
Xueyan He ◽  
Lai Chen ◽  
Chenxi Zhang ◽  
Xiang Gao ◽  
...  
Keyword(s):  
Heart Development ◽  
Endocardial Cushion ◽  
Synergistic Regulation ◽  
Endocardial Cushion Morphogenesis

scholarly journals FRS2α-dependent cell fate transition during endocardial cushion morphogenesis

2020 ◽  
Vol 458 (1) ◽  
pp. 88-97
Author(s):  
Dongying Chen ◽  
Xiaolong Zhu ◽  
Natalie Kofler ◽  
Yidong Wang ◽  
Bin Zhou ◽  
...  
Keyword(s):  
Cell Fate ◽  
Endocardial Cushion ◽  
Dependent Cell ◽  
Endocardial Cushion Morphogenesis

scholarly journals Expression of bone morphogenetic protein-5 gene during chick heart development: Possible roles in valvuloseptal endocardial cushion formation

2001 ◽  
Vol 264 (4) ◽  
pp. 313-316 ◽  
Author(s):  
Toshiyuki Yamagishi ◽  
Yuji Nakajima ◽  
Shin-Ichiro Nishimatsu ◽  
Tsutomu Nohno ◽  
Katsumi Ando ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Heart Development ◽  
Endocardial Cushion ◽  
Morphogenetic Protein ◽  
Chick Heart

A novel role for VEGF in endocardial cushion formation and its potential contribution to congenital heart defects

Development ◽  
2001 ◽  
Vol 128 (9) ◽  
pp. 1531-1538 ◽  
Author(s):  
Y. Dor ◽  
T.D. Camenisch ◽  
A. Itin ◽  
G.I. Fishman ◽  
J.A. McDonald ◽  
...  
Keyword(s):  
Growth Factor ◽  
Heart Development ◽  
Heart Defects ◽  
Negative Regulator ◽  
Congenital Defects ◽  
Endocardial Cushion ◽  
Potential Contribution ◽  
Vegf Receptor ◽  
Endocardial Cushions ◽  
Mesenchymal Transformation

Normal cardiovascular development is exquisitely dependent on the correct dosage of the angiogenic growth factor and vascular morphogen vascular endothelial growth factor (VEGF). However, cardiac expression of VEGF is also robustly augmented during hypoxic insults, potentially mediating the well-established teratogenic effects of hypoxia on heart development. We report that during normal heart morphogenesis VEGF is specifically upregulated in the atrioventricular (AV) field of the heart tube soon after the onset of endocardial cushion formation (i.e. the endocardium-derived structures that build the heart septa and valves). To model hypoxia-dependent induction of VEGF in vivo, we conditionally induced VEGF expression in the myocardium using a tetracycline-regulated transgenic system. Premature induction of myocardial VEGF in E9.5 embryos to levels comparable with those induced by hypoxia prevented formation of endocardial cushions. When added to explanted embryonic AV tissue, VEGF fully inhibited endocardial-to-mesenchymal transformation. Transformation was also abrogated in AV explants subjected to experimental hypoxia but fully restored in the presence of an inhibitory soluble VEGF receptor 1 chimeric protein. Together, these results suggest a novel developmental role for VEGF as a negative regulator of endocardial-to-mesenchymal transformation that underlies the formation of endocardial cushions. Moreover, ischemia-induced VEGF may be the molecular link between hypoxia and congenital defects in heart septation.

scholarly journals Temporal and Distinct TGFβ Ligand Requirements during Mouse and Avian Endocardial Cushion Morphogenesis

2002 ◽  
Vol 248 (1) ◽  
pp. 170-181 ◽  
Author(s):  
Todd D. Camenisch ◽  
Daniël G.M. Molin ◽  
Anthony Person ◽  
Raymond B. Runyan ◽  
Adriana C. Gittenberger-de Groot ◽  
...  
Keyword(s):  
Endocardial Cushion ◽  
Endocardial Cushion Morphogenesis

scholarly journals The W-Loop of Alpha-Cardiac Actin Is Critical for Heart Function and Endocardial Cushion Morphogenesis in Zebrafish

2012 ◽  
Vol 32 (17) ◽  
pp. 3527-3540 ◽  
Author(s):  
N. O. Glenn ◽  
M. McKane ◽  
V. Kohli ◽  
K.-K. Wen ◽  
P. A. Rubenstein ◽  
...  
Keyword(s):  
Heart Function ◽  
Endocardial Cushion ◽  
Cardiac Actin ◽  
Endocardial Cushion Morphogenesis

scholarly journals NOX2 Is Critical to Endocardial to Mesenchymal Transition and Heart Development

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Hoda Moazzen ◽  
Yan Wu ◽  
Anish Engineer ◽  
Xiangru Lu ◽  
Simran Aulakh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Heart Development ◽  
Ex Vivo ◽  
Heart Defects ◽  
Embryonic Heart ◽  
Abnormal Development ◽  
Endocardial Cushion ◽  
Atrioventricular Canal ◽  
Mesenchymal Transition ◽  
Septal Defects

NADPH oxidases (NOX) are a major source of reactive oxygen species (ROS) production in the heart. ROS signaling regulates gene expression, cell proliferation, apoptosis, and migration. However, the role of NOX2 in embryonic heart development remains elusive. We hypothesized that deficiency of Nox2 disrupts endocardial to mesenchymal transition (EndMT) and results in congenital septal and valvular defects. Our data show that 34% of Nox2-/- neonatal mice had various congenital heart defects (CHDs) including atrial septal defects (ASD), ventricular septal defects (VSD), atrioventricular canal defects (AVCD), and malformation of atrioventricular and aortic valves. Notably, Nox2-/- embryonic hearts show abnormal development of the endocardial cushion as evidenced by decreased cell proliferation and an increased rate of apoptosis. Additionally, Nox2 deficiency disrupted EndMT of atrioventricular cushion explants ex vivo. Furthermore, treatment with N-acetylcysteine (NAC) to reduce ROS levels in the wild-type endocardial cushion explants decreased the number of cells undergoing EndMT. Importantly, deficiency of Nox2 was associated with reduced expression of Gata4, Tgfβ2, Bmp2, Bmp4, and Snail1, which are critical to endocardial cushion and valvoseptal development. We conclude that NOX2 is critical to EndMT, endocardial cushion cell proliferation, and normal embryonic heart development.

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