{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Al-Radi O"],"funding":["EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions)","Vetenskapsrådet (Swedish Research Council)"],"pagination":["883"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12698774"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["The cell cycle is a key regulator of endothelial cell specification into tip and stalk cell phenotypes, which are essential for angiogenesis in both normal development and pathological conditions. While the tumor suppressor p53 is known to regulate the cell cycle and influence cell fate, its role in modulating the cell fate of these phenotypes remains unclear. Using non-genotoxic small molecule and stapled peptide compounds to pharmacologically activate p53 via MDM2 inhibition, we demonstrate that graded levels of p53 induce distinct cellular fates in normal endothelial cells. Low levels of p53 induce reversible cell cycle arrest by reducing DNA replication, while high levels induce senescence and cell death. Surprisingly, all tested levels of p53 activation reduced the growth of venous bl"],"journal":["Cell death & disease"],"pubmed_title":["Pharmacological activation of p53 induces dose-dependent changes in endothelial cell fate during angiogenic sprouting."],"pmcid":["PMC12698774"],"funding_grant_id":["2013-08807","839585"],"pubmed_authors":["Ingelshed K","Vegvari A","Al-Radi O","Cerrato CP","Lindstrom S","Krkoska M","Kheder S","Kannan P","Levander F","Bosdotter C","Ferme S","Eichhorn L","Brautigam L","Vojtesek B","Lane DP","Josefsson H","Allalou A"],"additional_accession":[]},"is_claimable":false,"name":"Pharmacological activation of p53 induces dose-dependent changes in endothelial cell fate during angiogenic sprouting.","description":"The cell cycle is a key regulator of endothelial cell specification into tip and stalk cell phenotypes, which are essential for angiogenesis in both normal development and pathological conditions. While the tumor suppressor p53 is known to regulate the cell cycle and influence cell fate, its role in modulating the cell fate of these phenotypes remains unclear. Using non-genotoxic small molecule and stapled peptide compounds to pharmacologically activate p53 via MDM2 inhibition, we demonstrate that graded levels of p53 induce distinct cellular fates in normal endothelial cells. Low levels of p53 induce reversible cell cycle arrest by reducing DNA replication, while high levels induce senescence and cell death. Surprisingly, all tested levels of p53 activation reduced the growth of venous bl","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-06T01:56:16.556Z","creation":"2026-05-24T03:12:22.877Z"},"accession":"S-EPMC12698774","cross_references":{"pubmed":["41360924"],"doi":["10.1038/s41419-025-08292-7"]}}