Endothelial Cell-Selective Adhesion Molecule Contributes to the Development of Definitive Hematopoiesis in the Fetal Liver.
definitive hematopoiesis
endothelial cell-selective adhesion molecule
endothelial cells
fetal liver
hematopoietic stem cells
Journal
Stem cell reports
ISSN: 2213-6711
Titre abrégé: Stem Cell Reports
Pays: United States
ID NLM: 101611300
Informations de publication
Date de publication:
10 12 2019
10 12 2019
Historique:
received:
14
02
2019
revised:
04
11
2019
accepted:
06
11
2019
pubmed:
10
12
2019
medline:
1
7
2020
entrez:
10
12
2019
Statut:
ppublish
Résumé
Endothelial cell-selective adhesion molecule (ESAM) is a lifelong marker of hematopoietic stem cells (HSCs). Although we previously elucidated the functional importance of ESAM in HSCs in stress-induced hematopoiesis in adults, it is unclear how ESAM affects hematopoietic development during fetal life. To address this issue, we analyzed fetuses from conventional or conditional ESAM-knockout mice. Approximately half of ESAM-null fetuses died after mid-gestation due to anemia. RNA sequencing analyses revealed downregulation of adult-type globins and Alas2, a heme biosynthesis enzyme, in ESAM-null fetal livers. These abnormalities were attributed to malfunction of ESAM-null HSCs, which was demonstrated in culture and transplantation experiments. Although crosslinking ESAM directly influenced gene transcription in HSCs, observations in conditional ESAM-knockout fetuses revealed the critical involvement of ESAM expressed in endothelial cells in fetal lethality. Thus, we showed that ESAM had important roles in developing definitive hematopoiesis. Furthermore, we unveiled the importance of endothelial ESAM in this process.
Identifiants
pubmed: 31813828
pii: S2213-6711(19)30405-9
doi: 10.1016/j.stemcr.2019.11.002
pmc: PMC6915804
pii:
doi:
Substances chimiques
Biomarkers
0
Cell Adhesion Molecules
0
Esam protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
992-1005Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
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