Endocardially Derived Macrophages Are Essential for Valvular Remodeling.
cardiac tissue macrophage
cardiogenesis
congenital heart disease
hematopoiesis
hemogenic endocardium
multipotent cardiac progenitor cells
tissue macrophages
valve disease
valve remodeling
valvulogenesis
Journal
Developmental cell
ISSN: 1878-1551
Titre abrégé: Dev Cell
Pays: United States
ID NLM: 101120028
Informations de publication
Date de publication:
11 03 2019
11 03 2019
Historique:
received:
05
09
2018
revised:
06
12
2018
accepted:
22
01
2019
pubmed:
26
2
2019
medline:
29
8
2019
entrez:
26
2
2019
Statut:
ppublish
Résumé
During mammalian embryogenesis, de novo hematopoiesis occurs transiently in multiple anatomical sites including the yolk sac, dorsal aorta, and heart tube. A long-unanswered question is whether these local transient hematopoietic mechanisms are essential for embryonic growth. Here, we show that endocardial hematopoiesis is critical for cardiac valve remodeling as a source of tissue macrophages. Colony formation assay from explanted heart tubes and genetic lineage tracing with the endocardial specific Nfatc1-Cre mouse revealed that hemogenic endocardium is a de novo source of tissue macrophages in the endocardial cushion, the primordium of the cardiac valves. Surface marker characterization, gene expression profiling, and ex vivo phagocytosis assay revealed that the endocardially derived cardiac tissue macrophages play a phagocytic and antigen presenting role. Indeed, genetic ablation of endocardially derived macrophages caused severe valve malformation. Together, these data suggest that transient hemogenic activity in the endocardium is indispensable for the valvular tissue remodeling in the heart.
Identifiants
pubmed: 30799229
pii: S1534-5807(19)30049-8
doi: 10.1016/j.devcel.2019.01.021
pmc: PMC6440481
mid: NIHMS1519567
pii:
doi:
Substances chimiques
NFATC Transcription Factors
0
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
617-630.e3Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL129727
Pays : United States
Organisme : NIGMS NIH HHS
ID : R25 GM055052
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR075867
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL118650
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL127427
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL111437
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL137241
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL129178
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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