Selective Activation of the Prostaglandin E₂Circuit in Chronic Injury-Induced Pathologic Angiogenesis

Abstract

These findings place the corneal PGE(2) circuit as an endogenous mediator of inflammatory neovascularization rather than general inflammation and demonstrate that chronic inflammation selectively regulates this circuit at the level of biosynthetic enzyme and receptor expression.

Suppression of Laser-Induced Choroidal Neovascularization by a CCR3 Antagonist

“…14 The CCR3-eotaxin axis is a newly identified pathway that contributes to ocular pathological angiogenesis, not only in CNV 13,29 but also in corneal angiogenesis. 30 The CCR3-eotaxin pathway has been reported to directly induce angiogenic responses in human, mouse, rat, and chick endothelial cells. 31 In vitro, eotaxin induced human endothelial cell migration in a dose-responsive manner that was correlated with CCR3 expression at the RNA and protein levels.…”

“…31 In vitro, eotaxin induced human endothelial cell migration in a dose-responsive manner that was correlated with CCR3 expression at the RNA and protein levels. 31 In a corneal neovascularization model, Liclican et al 30 showed that inflammatory neovascularization with prostaglandin E2 was independent of the VEGF circuit, and was instead associated with significant induction of the CCR3-eotaxin pathway. In agreement with their report, our experiments showed that CNV suppression by the CCR3 antagonist was independent of the total VEGF expression, and that the CCR3 antagonist suppressed eotaxin expression after the laser injury.…”

Suppression of Retinal Neovascularization by Anti-CCR3 Treatment in an Oxygen-Induced Retinopathy Model in Mice

“…Although the CCR3-eotaxin pathway has been shown to be involved in ocular pathological angiogenesis in choroidal neovascularization (CNV) [11][12][13][22][23][24] and in corneal angiogenesis [9,10] , to our knowledge, this is the first report to dem- onstrate a role for CCR3-eotaxin pathways in retinal neovascularization. Historically, the CCR3-eotaxin pathway has been known to contribute to eosinophil migration in allergic reactions [25] .…”

“…ciated with pathological angiogenic processes [9][10][11][12] . CCR3 has been related to injury-induced corneal angiogenesis [9,10] and to laser-induced choroidal neovascularization in a mouse experimental model [11][12][13] .…”

“…CCR3 has been related to injury-induced corneal angiogenesis [9,10] and to laser-induced choroidal neovascularization in a mouse experimental model [11][12][13] . To our knowledge, there is no previous report of an association between CCR3 and retinal neovascularization.…”