Endothelial cells and Leptin Receptor+ cells promote the maintenance of stem cells and hematopoiesis in early postnatal murine bone marrow

Mammalian hematopoietic stem cells (HSCs) colonize the bone marrow during late fetal development and this becomes the major site of hematopoiesis after birth. However, little is known about the early postnatal bone marrow niche. We performed single cell RNA-sequencing of mouse bone marrow stromal ce...

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Veröffentlicht in:Developmental cell 2023-03, Vol.58 (5), p.348-360.e6
Hauptverfasser: Kara, Nergis, Xue, Yuanyuan, Zhao, Zhiyu, Murphy, Malea M., Comazzetto, Stefano, Lesser, Ashley, Du, Liming, Morrison, Sean J.
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Sprache:eng
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Zusammenfassung:Mammalian hematopoietic stem cells (HSCs) colonize the bone marrow during late fetal development and this becomes the major site of hematopoiesis after birth. However, little is known about the early postnatal bone marrow niche. We performed single cell RNA-sequencing of mouse bone marrow stromal cells at 4 days, 14 days, and 8 weeks after birth. Leptin Receptor-expressing (LepR + ) stromal cells and endothelial cells increased in frequency during this period and changed their properties. At all postnatal stages, LepR + cells and endothelial cells expressed the highest Stem Cell Factor ( Scf ) levels in the bone marrow. LepR + cells expressed the highest Cxcl12 levels. In early postnatal bone marrow, SCF from LepR + /Prx1 + stromal cells promoted myeloid and erythroid progenitor maintenance while SCF from endothelial cells promoted HSC maintenance. Membrane bound SCF in endothelial cells contributed to HSCs maintenance. LepR + cells and endothelial cells are thus important niche components in early postnatal bone marrow. LepR+ stromal cells and endothelial cells express the highest Scf levels in early postnatal bone marrow. Kara and Xue et al. show these cells are necessary sources of SCF for progenitors and HSCs in early postnatal bone marrow and that they change their properties in the weeks after birth.
ISSN:1534-5807
1878-1551
DOI:10.1016/j.devcel.2023.02.003