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Nat Cell Biol. 2017 Mar;19(3):189-201. doi: 10.1038/ncb3476. Epub 2017 Feb 20.

Cell-matrix signals specify bone endothelial cells during developmental osteogenesis.

Author information

1
Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, D-48149 Münster, Germany.
2
Max Planck Institute for Molecular Biomedicine, Research Group Regulatory Genomics, D-48149 Münster, Germany.
3
Institute of Physiological Chemistry and Pathobiochemistry and Cells-in-Motion Cluster of Excellence, University of Münster, D-48149 Münster, Germany.
4
Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Abstract

Blood vessels in the mammalian skeletal system control bone formation and support haematopoiesis by generating local niche environments. While a specialized capillary subtype, termed type H, has been recently shown to couple angiogenesis and osteogenesis in adolescent, adult and ageing mice, little is known about the formation of specific endothelial cell populations during early developmental endochondral bone formation. Here, we report that embryonic and early postnatal long bone contains a specialized endothelial cell subtype, termed type E, which strongly supports osteoblast lineage cells and later gives rise to other endothelial cell subpopulations. The differentiation and functional properties of bone endothelial cells require cell-matrix signalling interactions. Loss of endothelial integrin β1 leads to endothelial cell differentiation defects and impaired postnatal bone growth, which is, in part, phenocopied by endothelial cell-specific laminin α5 mutants. Our work outlines fundamental principles of vessel formation and endothelial cell differentiation in the developing skeletal system.

PMID:
28218908
PMCID:
PMC5580829
DOI:
10.1038/ncb3476
[Indexed for MEDLINE]
Free PMC Article

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