Inhibition of corneal neovascularization by genetic ablation of CCR2.
OBJECTIVE
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.
Ambati
Balamurali K
BK
Department of Ophthalmology, Medical College of Georgia, Augusta, 30907, USA. bambati@mail.mcg.edu
Joussen
Antonia M
AM
Kuziel
William A
WA
Adamis
Anthony P
AP
Ambati
Jayakrishna
J
D000818:Animals; D003315:Cornea / Q000098:blood supply*; D017353:Gene Deletion; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018919:Neovascularization, Physiologic / Q000235:genetics* / Q000502:physiology; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000235:genetics* / Q000502:physiology
C515335:Ccr2 protein, mouse; D054390:Receptors, CCR2; D019707:Receptors, Chemokine