Sox7-positive endothelial progenitors establish coronary arteries and govern ventricular compaction.
SOX transcription factor
arterial cell fate
coronary vessels
heart development
non-compaction cardiomyopathy
Journal
EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049
Informations de publication
Date de publication:
09 10 2023
09 10 2023
Historique:
revised:
12
07
2023
received:
14
03
2022
accepted:
24
07
2023
medline:
10
10
2023
pubmed:
8
8
2023
entrez:
8
8
2023
Statut:
ppublish
Résumé
The cardiac endothelium influences ventricular chamber development by coordinating trabeculation and compaction. However, the endothelial-specific molecular mechanisms mediating this coordination are not fully understood. Here, we identify the Sox7 transcription factor as a critical cue instructing cardiac endothelium identity during ventricular chamber development. Endothelial-specific loss of Sox7 function in mice results in cardiac ventricular defects similar to non-compaction cardiomyopathy, with a change in the proportions of trabecular and compact cardiomyocytes in the mutant hearts. This phenotype is paralleled by abnormal coronary artery formation. Loss of Sox7 function disrupts the transcriptional regulation of the Notch pathway and connexins 37 and 40, which govern coronary arterial specification. Upon Sox7 endothelial-specific deletion, single-nuclei transcriptomics analysis identifies the depletion of a subset of Sox9/Gpc3-positive endocardial progenitor cells and an increase in erythro-myeloid cell lineages. Fate mapping analysis reveals that a subset of Sox7-null endothelial cells transdifferentiate into hematopoietic but not cardiomyocyte lineages. Our findings determine that Sox7 maintains cardiac endothelial cell identity, which is crucial to the cellular cross-talk that drives ventricular compaction and coronary artery development.
Identifiants
pubmed: 37551717
doi: 10.15252/embr.202255043
pmc: PMC10561369
doi:
Substances chimiques
Sox7 protein, mouse
0
SOXF Transcription Factors
0
Banques de données
GEO
['GSE231636', 'GSE236846']
Dryad
['10.5061/dryad.qv9s4mwm3']
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e55043Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL128503
Pays : United States
Informations de copyright
© 2023 The Authors. Published under the terms of the CC BY 4.0 license.
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