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E. L. Liclican, A. J. Leedom, A. Sullivan, K. Gronert; Evidence for Prostaglandin E2 as a Prominent and Specific Mediator of Corneal Inflammatory Neovascularization. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4959.
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Prostaglandin E2 is a key mediator of inflammation that is upregulated in numerous inflammatory diseases. It has pleiotropic and sometimes opposing bioactions that are receptor and tissue specific. Even though PGE2 has been detected in the eye during inflammation, the role of this prominent prostanoid and primary therapeutic target, surprisingly remains largely unexplored in the eye. Hence, we examined the role of PGE2 in two distinct models, namely, acute self-resolving inflammation or chronic inflammation with neovascularization.
Acute self-resolving inflammation was induced in anesthetized mice by epithelial abrasion, while chronic inflammation and neovascularization was induced for 7 days using the corneal suture model. Re-epithelialization was monitored by fluorescein staining and quantified by image analysis. Neovascularization was quantified by vital microscopy and immunofluorescence using CD31 as an endothelial marker. Myeloperoxidase activity was selected as a quantitative marker of PMN infiltration. Corneal PGE2 formation was analyzed by lipidomics. Mice were treated with PGE2 (100 ng topically, t.i.d.) for up to 7 days.
Lipidomic analyses demonstrated that corneal levels of PGE2 increased 5-fold and 11-fold on days 2 and 7, respectively, in the suture-induced chronic inflammation, which correlated with marked neovascularization. In contrast, corneal levels of PGE2 demonstrated no significant changes in the self-resolving abrasion injury. Moreover, topical PGE2 treatment exacerbated inflammatory neovascularization (121 ± 15% increase), but did not affect wound healing or PMN infiltration after epithelial injury.
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