title: ADP-ribosylation factor as a novel target for corneal neovascularization regression.
abstract: OBJECTIVE
  To evaluate the roles of ADP-ribosylation factor (ARF) in alkali-induced corneal neovascularization (CNV).
  
  
  METHODS
  CNV was induced by alkali injury and compared in ARF1 inhibitor- or vehicle-treated mice 3 weeks after injury. Angiogenic and apoptosis factor expression in corneas after injury was quantified with reverse-transcription PCR. Human retinal endothelial cell apoptosis induced by ARF1 inhibitor was detected with flow cytometry.
  
  
  RESULTS
  The mRNA expression of ARF1 was augmented in the corneas after alkali injury. Compared with vehicle-treated mice, ARF1 inhibitor-treated mice exhibited impaired CNV 3 weeks after injury, as evidenced by corneal whole mount CD31-staining. Concomitantly, the enhancement of intraocular vascular endothelial growth factor expression was reduced in ARF1 inhibitor-treated mice compared to control mice after injury. Moreover, local administration of the ARF1 inhibitor after alkali injury enhanced intraocular caspase-3 expression. ARF1 inhibitor treatment can significantly induce human retinal endothelial cell apoptosis.
  
  
  CONCLUSIONS
  The ARF1 inhibitor can induce the regression of alkali-induced CNV through increased endothelial cell apoptosis and downregulated intracorneal VEGF expression. ARF1 is an effective intervention target for CNV.
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, China PR.
authors.forename: Chunyan
authors.initials: C
authors.lastname: Dai
authors.forename: Gaoqin
authors.initials: G
authors.lastname: Liu
authors.forename: Longbiao
authors.initials: L
authors.lastname: Li
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Xiao
authors.forename: Xueguang
authors.initials: X
authors.lastname: Zhang
authors.forename: Peirong
authors.initials: P
authors.lastname: Lu
mesh_terms: D020823:ADP-Ribosylation Factor 1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D000468:Alkalies; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D003315:Cornea / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005434:Flow Cytometry; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D012160:Retina / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D000468:Alkalies; D004791:Enzyme Inhibitors; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; C505409:Casp3 protein, mouse; D053148:Caspase 3; D020823:ADP-Ribosylation Factor 1