scholarly journals Endocardial-to-mesenchymal transformation and mesenchymal cell colonization at the onset of human cardiac valve development

Development ◽  
2015 ◽  
Vol 143 (3) ◽  
pp. 473-482 ◽  
Author(s):  
Michael G. Monaghan ◽  
Miriam Linneweh ◽  
Simone Liebscher ◽  
Ben Van Handel ◽  
Shannon L. Layland ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Shimizu ◽  
Kazuaki Maruyama ◽  
Takeshi Kawamura ◽  
Yoshihiro Urade ◽  
Youichiro Wada

An amendment to this paper has been published and can be accessed via a link at the top of the paper.



2020 ◽  
Vol 126 (8) ◽  
pp. 968-984 ◽  
Author(s):  
Felix Gunawan ◽  
Alessandra Gentile ◽  
Sébastien Gauvrit ◽  
Didier Y.R. Stainier ◽  
Anabela Bensimon-Brito


2012 ◽  
Vol 4 (1) ◽  
pp. 92
Author(s):  
Gaëlle Odelin ◽  
Frank Kober ◽  
Jean François Avierinos ◽  
Sarah Arab ◽  
Piotr Topilko ◽  
...  


Development ◽  
2013 ◽  
Vol 140 (11) ◽  
pp. 2345-2353 ◽  
Author(s):  
M. Votteler ◽  
D. A. C. Berrio ◽  
A. Horke ◽  
L. Sabatier ◽  
D. P. Reinhardt ◽  
...  


2011 ◽  
Vol 91 (6) ◽  
pp. 449-459 ◽  
Author(s):  
Donal MacGrogan ◽  
Luis Luna-Zurita ◽  
José Luis de la Pompa


2016 ◽  
Author(s):  
Ryo Iwamoto ◽  
Naoki Mine ◽  
Hiroto Mizushima ◽  
Eisuke Mekada

AbstractHB-EGF plays an indispensable role in suppression of cell proliferation in mouse valvulogenesis. However, ligands of the EGF receptor (EGFR/ErbB1), including HB-EGF, are generally considered as growth-promoting factors, as shown in cancers. HB-EGF binds to and activates ErbB1 and ErbB4. We investigated the role of ErbB receptors in valvulogenesis in vivo using ErbB1- and ErbB4-deficient mice, and an ex vivo model of endocardial cushion explants. We show that HB-EGF suppresses valve mesenchymal cell proliferation through a heterodimer of ErbB1 and ErbB4, and an ErbB1 ligand(s) promotes cell proliferation through a homodimer of ErbB1. Moreover, a rescue experiment with cleavable or uncleavable isoforms of ErbB4 in ERBB4 null cells suggests that the cytoplasmic intracellular domain of ErbB4, rather than the membrane-anchored tyrosine kinase, achieves this suppression. Our study demonstrates that opposing signals generated by different ErbB dimer combinations function in the same cardiac cushion mesenchymal cells for proper cardiac valve formation.Summary statementIn valvulogenesis, opposing signals generated by different combinations of ErbB-dimers elaborately regulate cell proliferation, in which proteolytically released intracellular domain of ErbB4 activated by HB-EGF is required to suppress proliferation.



2017 ◽  
Vol 23 (S1) ◽  
pp. 1330-1331
Author(s):  
Vinal Menon ◽  
Lorain Junor ◽  
John Eberth ◽  
Stephanie Ford ◽  
Matt McPheeters ◽  
...  


2021 ◽  
Author(s):  
Lilong Guo ◽  
Tyler Beck ◽  
Diana Fulmer ◽  
Sandra Ramos‐Ortiz ◽  
Janiece Glover ◽  
...  


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