{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:10:52Z","timestamp":1762099852262},"reference-count":44,"publisher":"Rockefeller University Press","issue":"12","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,6,18]]},"abstract":"<jats:p>The requirement for the nonreceptor tyrosine kinase c-abl in the pathogenesis of retinopathy of prematurity (ROP) was examined using the mouse model for ROP and c-abl\u2013deficient mice. Hyperoxia-induced retinal neovascularization was observed in wild-type and heterozygous mice but animals that were homozygous null for c-abl did not develop a vasoproliferative retinopathy in response to hyperoxia. Two gene products, endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF), have been implicated in the pathogenesis of ROP. The mRNA expression of ET-1 and VEGF was assessed in mice maintained in normoxia and in hyperoxia-exposed mice. ET-1 mRNA levels were unchanged in wild-type mice throughout the hyperoxia treatment, suggesting that ET-1 mRNA expression is not regulated by the increase in inspired oxygen. In wild-type mice maintained in room air, VEGF mRNA levels rose threefold from postnatal day 6 (P6) to P17. When wild-type mice were treated with the hyperoxia regimen, a fivefold decrease in VEGF mRNA expression was observed from P7 to P16. However, retinal VEGF expression in hyperoxia-treated homozygous null mice did not decrease and remained at control levels. These data suggest that c-abl is required for the hyperoxia-induced retinal neovascularization and hyperoxia-induced decrease in VEGF mRNA levels.<\/jats:p>","DOI":"10.1084\/jem.193.12.1383","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:48:54Z","timestamp":1027702134000},"page":"1383-1392","update-policy":"http:\/\/dx.doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":10,"title":["C-Abl Is Required for the Development of Hyperoxia-Induced Retinopathy"],"prefix":"10.1084","volume":"193","author":[{"given":"Irene","family":"Nunes","sequence":"first","affiliation":[{"name":"aDepartment of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, New York 10032"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rosemary D.","family":"Higgins","sequence":"additional","affiliation":[{"name":"bDepartment of Pediatrics, Georgetown University, Washington, DC 20007"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucia","family":"Zanetta","sequence":"additional","affiliation":[{"name":"cDepartment of Surgery, New York University School of Medicine, New York, New York 10016"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Shamamian","sequence":"additional","affiliation":[{"name":"cDepartment of Surgery, New York University School of Medicine, New York, New York 10016"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen P.","family":"Goff","sequence":"additional","affiliation":[{"name":"aDepartment of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, New York 10032"},{"name":"dHoward Hughes Medical Institute, New York, New York 10032"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"291","published-online":{"date-parts":[[2001,6,18]]},"reference":[{"key":"2023072509350531900_R1","doi-asserted-by":"crossref","first-page":"50","DOI":"10.1542\/pir.16.2.50","article-title":"Retinopathy of prematurity","volume":"16","author":"Phelps","year":"1995","journal-title":"Pediatr. 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