FRS2α-dependent cell fate transition during endocardial cushion morphogenesis.
Animals
Cell Count
Cell Lineage
Endocardial Cushion Defects
/ embryology
Endocardial Cushions
/ cytology
Endothelial Cells
/ cytology
Gene Deletion
Gene Expression Regulation, Developmental
Membrane Proteins
/ deficiency
Mesoderm
/ cytology
Mice
Mice, Inbred C57BL
MicroRNAs
/ physiology
Mitral Valve
/ abnormalities
Morphogenesis
/ genetics
Phenotype
Tricuspid Valve
/ abnormalities
Cardiovascular development
Cell fate
EndMT
Endocardial cushion
Endothelial-to-mesenchymal transition
Valvulogenesis
Journal
Developmental biology
ISSN: 1095-564X
Titre abrégé: Dev Biol
Pays: United States
ID NLM: 0372762
Informations de publication
Date de publication:
01 02 2020
01 02 2020
Historique:
received:
04
07
2019
revised:
03
10
2019
accepted:
22
10
2019
pubmed:
2
11
2019
medline:
11
8
2020
entrez:
1
11
2019
Statut:
ppublish
Résumé
Atrioventricular valve development requires endothelial-to-mesenchymal transition (EndMT) that induces cushion endocardial cells to give rise to mesenchymal cells crucial to valve formation. In the adult endothelium, deletion of the docking protein FRS2α induces EndMT by activating TGFβ signaling in a miRNA let-7-dependent manner. To study the role of endothelial FRS2α during embryonic development, we generated mice with an inducible endothelial-specific deletion of Frs2α (FRS2α
Identifiants
pubmed: 31669335
pii: S0012-1606(19)30390-2
doi: 10.1016/j.ydbio.2019.10.022
pii:
doi:
Substances chimiques
FRS2alpha protein, mouse
0
Membrane Proteins
0
MicroRNAs
0
mirnlet7 microRNA, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
88-97Informations de copyright
Copyright © 2019. Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declaration of competing interest None.