title: Avastin treatment reduces retinal neovascularization in a mouse model of retinopathy of prematurity.
abstract: OBJECTIVE
  This study was designed to evaluate the effect of one intraperitoneal (IP) injection of bevacizumab (Avastin) on the severity of oxygen-induced retinopathy (OIR) in a mouse model.
  
  
  METHODS
  Twenty-eight eyes of 14 mice with OIR were studied. There were nine mice in the bevacizumab-treated group (study group) and five mice in the saline-treated group (controls). The mouse OIR model consisted of a 5-day exposure to 75% oxygen. On postnatal day 12 (P12), Avastin 2.5 mg/kg was administered IP to the study group and 2.5 mg/kg normal saline was administered IP to the controls. All 14 mice underwent fluorescein angiography of the retinal vasculature on P17 and the following parameters were scored (Modified Retinopathy Scoring System, MRSS): blood vessel growth, formation of blood vessel tufts, extraretinal neovascularization, degree of central constriction, and tortuosity of vessels. In addition, the neovascular vessels were quantified on the hematoxylin and eosin (H&S)-stained paraffin sections of the eyes in a masked fashion.
  
  
  RESULTS
  The MRSS score in the Avastin-treated mice was significantly lower than that of the saline-treated mice (3.06 ± 1.63 versus 7.1 ± 2.01, respectively, p = 0.0021). The neovascularization count was also significantly lower in the study group (3.44 ± 1.81 versus 9.34 ± 3.23 for the controls, p = 0.0013).
  
  
  CONCLUSIONS
  IP Avastin treatment reduced the extent of oxygen-induced retinopathy in a mouse model of retinopathy of prematurity.
authors.affiliation: Goldschleger Eye Institute, Tel-Aviv University , Tel-Aviv, Israel.
authors.forename: Ronen
authors.initials: R
authors.lastname: Rabinowitz
authors.forename: Ayelet
authors.initials: A
authors.lastname: Priel
authors.forename: Mordechai
authors.initials: M
authors.lastname: Rosner
authors.forename: Sara
authors.initials: S
authors.lastname: Pri-Chen
authors.forename: Abraham
authors.initials: A
authors.lastname: Spierer
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D000831:Animals, Newborn; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D000068258:Bevacizumab; D003911:Dextrans; D004195:Disease Models, Animal; D005451:Fluorescein Angiography; D005452:Fluoresceins; D006801:Humans; D007231:Infant, Newborn; D007274:Injections, Intraperitoneal; D051379:Mice; D008810:Mice, Inbred C57BL; D010100:Oxygen / Q000633:toxicity; D015861:Retinal Neovascularization / Q000175:diagnosis / Q000188:drug therapy*; D012171:Retinal Vessels / Q000473:pathology; D012178:Retinopathy of Prematurity / Q000175:diagnosis / Q000188:drug therapy*; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D003911:Dextrans; D005452:Fluoresceins; D042461:Vascular Endothelial Growth Factor A; C052526:fluorescein-dextran; C467480:vascular endothelial growth factor A, mouse; D000068258:Bevacizumab; D010100:Oxygen