{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wille A"],"funding":["Deutsche Forschungsgesellschaft","Deutsche Forschungsgemeinschaft","Else Kröner-Fresenius-Stiftung"],"pagination":["357-372"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11240155"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(3)"],"pubmed_abstract":["Sphingosine-1-phosphate (S1P) plays multiple roles in bone metabolism and regeneration. Here, we have identified a novel S1P-regulated osteoanabolic mechanism functionally connecting osteoblasts (OBs) to the highly specialized bone vasculature. We demonstrate that S1P/S1PR3 signaling in OBs stimulates vascular endothelial growth factor a (VEGFa) expression and secretion to promote bone growth in an autocrine and boost osteogenic H-type differentiation of bone marrow endothelial cells in a paracrine manner. VEGFa-neutralizing antibodies and VEGF receptor inhibition by axitinib abrogated OB growth in vitro and bone formation in male C57BL/6J in vivo following S1P stimulation and S1P lyase inhibition, respectively. Pharmacological S1PR3 inhibition and genetic S1PR3 deficiency suppressed VEGFa"],"journal":["Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research"],"pubmed_title":["Sphingosine-1-phosphate promotes osteogenesis by stimulating osteoblast growth and neovascularization in a vascular endothelial growth factor-dependent manner."],"pmcid":["PMC11240155"],"funding_grant_id":["LE 940/8-2","BE 4169/8-2","GRK2098","DFG- INST 208/746-1 FUGG"],"pubmed_authors":["Thomas N","Keul P","Deister-Jonas J","von Wnuck Lipinski K","Schroder NH","Nowak MK","Levkau B","Wille A","Weske S","Wollnitzke P","Behr B"],"additional_accession":[]},"is_claimable":false,"name":"Sphingosine-1-phosphate promotes osteogenesis by stimulating osteoblast growth and neovascularization in a vascular endothelial growth factor-dependent manner.","description":"Sphingosine-1-phosphate (S1P) plays multiple roles in bone metabolism and regeneration. Here, we have identified a novel S1P-regulated osteoanabolic mechanism functionally connecting osteoblasts (OBs) to the highly specialized bone vasculature. We demonstrate that S1P/S1PR3 signaling in OBs stimulates vascular endothelial growth factor a (VEGFa) expression and secretion to promote bone growth in an autocrine and boost osteogenic H-type differentiation of bone marrow endothelial cells in a paracrine manner. VEGFa-neutralizing antibodies and VEGF receptor inhibition by axitinib abrogated OB growth in vitro and bone formation in male C57BL/6J in vivo following S1P stimulation and S1P lyase inhibition, respectively. Pharmacological S1PR3 inhibition and genetic S1PR3 deficiency suppressed VEGFa","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2025-04-26T14:11:50.046Z","creation":"2025-04-06T14:31:01.811Z"},"accession":"S-EPMC11240155","cross_references":{"pubmed":["38477738"],"doi":["10.1093/jbmr/zjae006"]}}