Inhibition of corneal neovascularization by genetic ablation of CCR2

被引:38
作者
Ambati, BK [1 ]
Joussen, AM
Kuziel, WA
Adamis, AP
Ambati, J
机构
[1] Med Coll Georgia, Dept Ophthalmol, Augusta, GA 30907 USA
[2] Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Boston, MA 02114 USA
[3] Univ Cologne, Ctr Ophthalmol, Dept Vitreoretinal Surg, D-50931 Cologne, Germany
[4] Univ Texas, Sect Mol Genet & Microbiol, Austin, TX 78712 USA
[5] Univ Texas, Inst Cellular & Mol Biol, Austin, TX 78712 USA
[6] Eyetech Pharmaceut, Woburn, MA 01801 USA
[7] Univ Kentucky, Dept Ophthalmol, Lexington, KY 40536 USA
关键词
angiogenesis; neovascularization; cornea; CCR2; inhibition;
D O I
10.1097/00003226-200307000-00013
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose. To determine if genetic ablation of the chemokine receptor CCR2 (involved in leukocyte and endothelial chemotaxis) inhibits the development of corneal neovascularization. Methods. Wild-type C57BL/6J mice, as well as species-specific counterparts with targeted homozygous disruption of the CCR2. underwent chemical and mechanical denudation of corneal and limbal epithelium. Corneas were harvested 2 weeks after injury. Neovascularization was quantified by CD31 immunostaining. Results. The mean percentages of neovascularized corneal area in control mice and CCR2-deficient mice 2 weeks after denudation were 58.3% and 38.8% (P = 0.047), respectively. Conclusions. Development of corneal neovascularization is inhibited in CCR2-deficient mice.
引用
收藏
页码:465 / 467
页数:3
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