AIM To investigate the effect and mechanism of CCR3 signal on corneal neovascularization (CRNV) induced by alkali burn.
METHODS CRNV was induced by alkali injury in mice. The time kinetic CCR3 expression in burned corneas was examined by reverse transcription polymerase chain reaction (RT-PCR). CCR3-antagonist (SB-328437 at the concentration of 125 µg/ml, 250 µg/ml, and 500 µg/ml) was locally administrated after alkali injury and the formation of CRNV 2 weeks after injury was assessed by CD31 corneal whole mount staining. MCP-1, MCP-3 expressions in the early phase after injury were quantified and compared by RT-PCR. Macrophage intracorneal accumulation in the early phase after injury was evaluated and compared by immunohistochemistry.
RESULTS Alkali injury induced the time kinetic intracorneal CCR3 expression. 500 µg/ml of CCR3-antagonist treatment in the early phase but not the late phase resulted in significant impaired CRNV as compared to control group (P<0.05). CCR3-antagonist treatment in the early phase significantly reduced the intracorneal MCP-1 and MCP-3 enhancement compare to control group at day 2 and day 4 (P<0.05). Moreover, the number of intracorneal macrophage infiltration in the experimental group was reduced than those in control group at day 4 (P<0.05).
CONCLUSION CCR3 signal was involved in the alkali induced CRNV. CCR3-antagonist can inhibit alkali induced CRNV by reducing the intracorneal MCP-1 and MCP-3 mRNA expression and the intracorneal macrophage infiltration. |
