{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Seebauer CT"],"funding":["National Health and Medical Research Council Career Development Fellows","Deutsche Forschungsgemeinschaft (DFG) grant","NHLBI NIH HHS","National Health and Medical Research Council","National Institutes of Health"],"pagination":["e151109"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8803322"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(3)"],"pubmed_abstract":["Propranolol and atenolol, current therapies for problematic infantile hemangioma (IH), are composed of R(+) and S(-) enantiomers: the R(+) enantiomer is largely devoid of beta blocker activity. We investigated the effect of R(+) enantiomers of propranolol and atenolol on the formation of IH-like blood vessels from hemangioma stem cells (HemSCs) in a murine xenograft model. Both R(+) enantiomers inhibited HemSC vessel formation in vivo. In vitro, similar to R(+) propranolol, both atenolol and its R(+) enantiomer inhibited HemSC to endothelial cell differentiation. As our previous work implicated the transcription factor sex-determining region Y (SRY) box transcription factor 18 (SOX18) in propranolol-mediated inhibition of HemSC to endothelial differentiation, we tested in parallel a known "],"journal":["The Journal of clinical investigation"],"pubmed_title":["Non-beta blocker enantiomers of propranolol and atenolol inhibit vasculogenesis in infantile hemangioma."],"pmcid":["PMC8803322"],"funding_grant_id":["GNT1111169","SE 3066/1-1","R01 HL096384","GNT1164000","HL 096384-09"],"pubmed_authors":["Fontaine F","Karnezis T","Zurakowski D","Huang L","Wylie-Sears J","Graus MS","McCann A","Francois M","Seebauer CT","Meunier F","Staffa SJ","Mulliken JB","Bischoff J"],"additional_accession":[]},"is_claimable":false,"name":"Non-beta blocker enantiomers of propranolol and atenolol inhibit vasculogenesis in infantile hemangioma.","description":"Propranolol and atenolol, current therapies for problematic infantile hemangioma (IH), are composed of R(+) and S(-) enantiomers: the R(+) enantiomer is largely devoid of beta blocker activity. We investigated the effect of R(+) enantiomers of propranolol and atenolol on the formation of IH-like blood vessels from hemangioma stem cells (HemSCs) in a murine xenograft model. Both R(+) enantiomers inhibited HemSC vessel formation in vivo. In vitro, similar to R(+) propranolol, both atenolol and its R(+) enantiomer inhibited HemSC to endothelial cell differentiation. As our previous work implicated the transcription factor sex-determining region Y (SRY) box transcription factor 18 (SOX18) in propranolol-mediated inhibition of HemSC to endothelial differentiation, we tested in parallel a known ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-06-18T08:48:34.715Z","creation":"2025-04-19T13:19:34.336Z"},"accession":"S-EPMC8803322","cross_references":{"pubmed":["34874911"],"doi":["10.1172/JCI151109"]}}