{"entity": "researcher", "timestamp": "2026-08-23T11:36:43.137Z", "family": "Vestweber", "given": "Dietmar", "initials": "D", "orcid": "0000-0002-3517-732X", "affiliations": ["Max Planck Institute for Molecular Biomedicine, M\u00fcnster, Germany."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f301c4b5e7f44e5beda910d49315c50.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f301c4b5e7f44e5beda910d49315c50"}}, "publications": [{"entity": "publication", "iuid": "2d862b2b319c4ca798556d74ee34f863", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2d862b2b319c4ca798556d74ee34f863.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2d862b2b319c4ca798556d74ee34f863"}}, "title": "Vascular permeability in retinopathy is regulated by VEGFR2 Y949 signaling to VE-cadherin.", "authors": [{"family": "Smith", "given": "Ross O", "initials": "RO", "orcid": "0000-0003-4239-3204", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f597e3f2a2a142c5b0dc7e1559f800b7.json"}}, {"family": "Ninchoji", "given": "Takeshi", "initials": "T"}, {"family": "Gordon", "given": "Emma", "initials": "E"}, {"family": "Andr\u00e9", "given": "Helder", "initials": "H"}, {"family": "Dejana", "given": "Elisabetta", "initials": "E"}, {"family": "Vestweber", "given": "Dietmar", "initials": "D", "orcid": "0000-0002-3517-732X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f301c4b5e7f44e5beda910d49315c50.json"}}, {"family": "Kvanta", "given": "Anders", "initials": "A"}, {"family": "Claesson-Welsh", "given": "Lena", "initials": "L", "orcid": "0000-0003-4275-2000", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6b07fbf00dad4ac8a4a53402888d55ef.json"}}], "type": "journal article", "published": "2020-04-21", "journal": {"title": "Elife", "issn": "2050-084X", "volume": "9", "issn-l": "2050-084X"}, "abstract": "Edema stemming from leaky blood vessels is common in eye diseases such as age-related macular degeneration and diabetic retinopathy. Whereas therapies targeting vascular endothelial growth factor A (VEGFA) can suppress leakage, side-effects include vascular rarefaction and geographic atrophy. By challenging mouse models representing different steps in VEGFA/VEGF receptor 2 (VEGFR2)-induced vascular permeability, we show that targeting signaling downstream of VEGFR2 pY949 limits vascular permeability in retinopathy induced by high oxygen or by laser-wounding. Although suppressed permeability is accompanied by reduced pathological neoangiogenesis in oxygen-induced retinopathy, similarly sized lesions leak less in mutant mice, separating regulation of permeability from angiogenesis. Strikingly, vascular endothelial (VE)-cadherin phosphorylation at the Y685, but not Y658, residue is reduced when VEGFR2 pY949 signaling is impaired. These findings support a mechanism whereby VE-cadherin Y685 phosphorylation is selectively associated with excessive vascular leakage. Therapeutically, targeting VEGFR2-regulated VE-cadherin phosphorylation could suppress edema while leaving other VEGFR2-dependent functions intact.", "doi": "10.7554/eLife.54056", "pmid": "32312382", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7188482"}, {"db": "pii", "key": "54056"}], "notes": [], "created": "2026-08-21T13:07:32.230Z", "modified": "2026-08-21T13:07:32.366Z"}]}