Targeting skeletal endothelium to ameliorate bone loss.

ABSTRACT: Recent studies have identified a specialized subset of CD31^hiendomucin^hi (CD31^hiEMCN^hi) vascular endothelium that positively regulates bone formation. However, it remains unclear how CD31^hiEMCN^hi endothelium levels are coupled to anabolic bone formation. Mice with an osteoblast-specific deletion of Shn3, which have markedly elevated bone formation, demonstrated an increase in CD31^hiEMCN^hi endothelium. Transcriptomic analysis identified SLIT3 as an osteoblast-derived, SHN3-regulated proangiogenic factor. Genetic deletion of Slit3 reduced skeletal CD31^hiEMCN^hi endothelium, resulted in low bone mass because of impaired bone formation and partially reversed the high bone mass phenotype

SUBMITTER: Xu R 

PROVIDER: S-EPMC5992080 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature