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Updated: Feb 24, 2026
The Corneal Micropocket Assay: A Model of Angiogenesis in the Mouse Eye
Published on: August 16, 2014
Genome-wide expression differences in anti-Vegf and dexamethasone treatment of inflammatory angiogenesis in the rat
Pierfrancesco Mirabelli1, Anthony Mukwaya1, Anton Lennikov1
1Department of Ophthalmology, Institute for Clinical and Experimental Medicine,Faculty of Health Sciences, Linkoping University, 58183, Linköping, Sweden.
Abstract:
Angiogenesis as a pathological process in the eye can lead to blindness. In the cornea, suppression of angiogenesis by anti-VEGF treatment is only partially effective while steroids, although effective in treating inflammation and angiogenesis, have broad activity leading to undesirable side effects. In this study, genome-wide expression was investigated in a suture-induced corneal neovascularization model in rats, to investigate factors differentially targeted by dexamethasone and anti-Vegf. Topical treatment with either rat-specific anti-Vegf, dexamethasone, or normal goat IgG (sham) was given to sutured corneas for 48 hours, after which in vivo imaging, tissue processing for RNA microarray, and immunofluorescence were performed. Dexamethasone suppressed limbal vasodilation (P < 0.01) and genes in PI3K-Akt, focal adhesion, and chemokine signaling pathways more effectively than anti-Vegf. The most differentially expressed genes were confirmed by immunofluorescence, qRTPCR and Western blot. Strong suppression of Reg3g and the inflammatory chemokines Ccl2 and Cxcl5 and activation of classical complement pathway factors C1r, C1s, C2, and C3 occurred with dexamethasone treatment, effects absent with anti-Vegf treatment. The genome-wide results obtained in this study provide numerous potential targets for specific blockade of inflammation and angiogenesis in the cornea not addressed by anti-Vegf treatment, as possible alternatives to broad-acting immunosuppressive therapy.
Insights
Dexamethasone more effectively suppressed corneal angiogenesis and inflammation than anti-VEGF treatments by targeting specific pathways. This study identifies new therapeutic targets for eye conditions, offering alternatives to broad immunosuppressants.
Area of Science:
- Ophthalmology
- Molecular Biology
- Immunology
Background:
- Pathological ocular angiogenesis contributes to blindness.
- Current treatments like anti-VEGF and steroids have limitations, including partial efficacy and broad side effects.
Purpose of the Study:
- To investigate genome-wide gene expression differences between dexamethasone and anti-VEGF treatments in a rat corneal neovascularization model.
- To identify novel therapeutic targets for corneal inflammation and angiogenesis.
Main Methods:
- A suture-induced corneal neovascularization model in rats was used.
- Topical treatments included rat-specific anti-VEGF, dexamethasone, and sham.
- Analysis involved in vivo imaging, RNA microarray, immunofluorescence, qRTPCR, and Western blot.
Main Results:
- Dexamethasone significantly suppressed limbal vasodilation and key signaling pathways (PI3K-Akt, focal adhesion, chemokine).
- Dexamethasone strongly suppressed Reg3g, Ccl2, and Cxcl5, and activated complement factors (C1r, C1s, C2, C3).
- These effects were largely absent with anti-VEGF treatment.
Conclusions:
- Dexamethasone targets distinct molecular pathways compared to anti-VEGF in corneal angiogenesis.
- Genome-wide analysis reveals numerous potential targets for specific blockade of corneal inflammation and angiogenesis.
- These findings suggest alternative therapeutic strategies beyond current anti-VEGF and broad immunosuppressive therapies.
