{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:48:13Z","timestamp":1782866893058,"version":"3.54.5"},"reference-count":62,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T00:00:00Z","timestamp":1757462400000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FASEB BioAdvances"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Vascular endothelial growth factor (VEGF) is important in both developmental and pathologic angiogenesis in retinopathy of prematurity (ROP). Using a rat model representative of ROP, we found that regulation of VEGF signaling through VEGF receptor 2 (VEGFR2) in retinal microvascular endothelial cells (RMVECs) extended developmental angiogenesis but reduced pathologic angiogenesis, that is, intravitreal neovascularization (IVNV). We identified an adaptor protein, MEMO1, in IVNV in the rat model and tested the hypothesis that MEMO1 in RMVECs was important in IVNV by regulating signaling through VEGFR2. Instead, we found MEMO1 knockdown enhanced phosphorylation of VEGF\u2010induced VEGFR2 and STAT3 and increased wound closure in\u00a0vitro using cultured human RMVECs. Furthermore, MEMO1 overexpression suppressed VEGF\u2010induced VEGFR2 and STAT3 phosphorylation and dampened VEGF\u2010induced RMVEC wound closure. In contrast, in the absence of VEGF, MEMO1 overexpression promoted RMVEC proliferation in the wound closure assay and AKT phosphorylation, supporting a role for MEMO1 in VEGF\u2010independent angiogenic processes. In\u00a0vivo, retinal endothelial cell\u2010specific knockdown of MEMO1 in the rat ROP model significantly increased IVNV but did not affect developmental angiogenesis. Our findings support a novel regulatory role for MEMO1 where MEMO1 limits VEGF\u2010driven IVNV and promotes VEGF\u2010independent angiogenic signaling. These results suggest MEMO1 may serve as a protective modulator of pathological angiogenesis in ROP and represent a potential therapeutic target to limit IVNV while preserving physiologic angiogenesis.<\/jats:p>","DOI":"10.1096\/fba.2025-00146","type":"journal-article","created":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T15:24:28Z","timestamp":1757517868000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Endothelial\n                    <scp>MEMO1<\/scp>\n                    Regulates Angiogenic Signaling in a Model of Retinopathy of Prematurity"],"prefix":"10.1096","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0599-4337","authenticated-orcid":false,"given":"Aniket","family":"Ramshekar","sequence":"first","affiliation":[{"name":"Department of Ophthalmology, Byers Eye Institute Stanford University School of Medicine  Stanford California USA"},{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bright","family":"Asare\u2010Bediako","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Byers Eye Institute Stanford University School of Medicine  Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jasmine","family":"Nguyen","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Byers Eye Institute Stanford University School of Medicine  Stanford California USA"},{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arundhathy","family":"Suresh","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Byers Eye Institute Stanford University School of Medicine  Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron","family":"Simmons","sequence":"additional","affiliation":[{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Colin A.","family":"Bretz","sequence":"additional","affiliation":[{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haibo","family":"Wang","sequence":"additional","affiliation":[{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Kunz","sequence":"additional","affiliation":[{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chandler J.","family":"Zaugg","sequence":"additional","affiliation":[{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris","family":"Wallace\u2010Carrete","sequence":"additional","affiliation":[{"name":"John A. Moran Eye Center University of Utah  Salt Lake City Utah USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. Elizabeth","family":"Hartnett","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Byers Eye Institute Stanford University School of Medicine  Stanford California USA"},{"name":"John A. 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