title: [Inhibited experimental mouse corneal neovascularization by CCR3 antagonist].
abstract: OBJECTIVE
  To explore the effect of CCR3 antagonist on the development of experimental corneal neovascularization.
  
  
  METHODS
  Mouse corneas were burned by NaOH to induce corneal neovascularization.Fifty four clean male BABL/c mice aged 7-8 weeks were divided into control group, CCR3 antagonist group and VEGF antibody positive group according to randomized number table. The gene expression of CCR3 and its ligand eotaxin in burned corneas was examined by Real-time PCR. CCR3 antagonist was locally administrated after alkali injury and the formation of corneal neovascular 2 weeks after injury was examined using a digital camera linked to a slit lamp microscope and corneal whole mount staining with CD31. The mRNA and protein expression of chemokines in burned corneas was detected by Real-time PCR and western blot.
  
  
  RESULTS
  Compared to control group, CCR3 antagonist treated mice resulted in significantly decreased corneal neovascularization. The related CNV area was 0.51 ± 0.03 in the CCR3 antagonist group, and that in the control group was 0.77 ± 0.15, with significant difference between them (t = 12.91, P = 0.00).Western blot detection did not show significant difference of VEGF protein expression between two groups.Expression level of VEGF in the CCR3 antagonist group was 0.91 ± 0.24, and that in the control group was 1.15 ± 0.30, showing no significant difference (t = 1.08, P = 0.34).
  
  
  CONCLUSIONS
  Alkali-induced corneal neovascularization was inhibited by CCR3 antagonist. The mechanism that CCR3 pathway plays an important role in corneal neovascularization needs further exploration.
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Gaoqin
authors.initials: G
authors.lastname: Liu
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Xuefei
authors.initials: X
authors.lastname: He
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Zhou
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Xiao
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Chen
authors.affiliation: Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China. Email: lupeirong@yahoo.com.hk.
authors.forename: Peirong
authors.initials: P
authors.lastname: Lu
mesh_terms: D000818:Animals; D002057:Burns, Chemical / Q000150:complications; D016510:Corneal Neovascularization / Q000139:chemically induced / Q000517:prevention & control*; D004195:Disease Models, Animal; D015870:Gene Expression; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D060888:Real-Time Polymerase Chain Reaction; D054397:Receptors, CCR3 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D012972:Sodium Hydroxide; D042461:Vascular Endothelial Growth Factor A
chemical_list: C515351:Ccr3 protein, mouse; D012333:RNA, Messenger; D054397:Receptors, CCR3; D042461:Vascular Endothelial Growth Factor A; D012972:Sodium Hydroxide