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The Corneal Micropocket Assay: A Model of Angiogenesis in the Mouse Eye
Published on: August 16, 2014
Macrophage inflammatory protein-2 and vascular endothelial growth factor regulate corneal neovascularization induced
Mei-Lang Xue1, Archana Thakur, Mark Willcox
1Cooperative Research Centre for Eye Research and Technology, School of Optometry and Vision Science, University of New South Wales, Sydney, New South Wales, Australia.
Abstract:
Pseudomonas aeruginosa ocular infection causes extensive corneal neovascularization. The purpose of the present study was to investigate the role of the angiogenic factors macrophage inflammatory protein-2 (MIP-2) and vascular endothelial growth factor (VEGF) in the regulation of corneal neovascularization during P. aeruginosa ocular infection. After administering anti-MIP-2 antibody or control antibody, mouse corneas were challenged with P. aeruginosa. The expression of MIP-2 and VEGF was detected using an ELISA from ocular homogenates. Corneal neovascularization was examined by histology. The cellular sources of MIP-2 and VEGF were identified by immunohistochemistry. In addition, protein expression of MIP-2 and VEGF in isolated corneas was measured to determine the ability of the cornea to produce these two mediators. Results showed that the expression of MIP-2 and VEGF was significantly (P < 0.05) elevated after bacterial infection, and high levels of these two mediators paralleled the extensive corneal neovascularization seen at later stages of the infection. Anti-MIP-2 antibody treatment resulted in a significant (P < 0.05) reduction in VEGF expression and in corneal neovascularization. Both corneal resident cells and infiltrating neutrophils had the ability to produce MIP-2 and VEGF after stimulation. The present study demonstrates that both MIP-2 and VEGF are important mediators in the regulation of corneal neovascularization caused by P. aeruginosa infection, and that MIP-2 regulates the production of VEGF.
Insights
Pseudomonas aeruginosa infection triggers corneal neovascularization. Blocking macrophage inflammatory protein-2 (MIP-2) reduced vascular endothelial growth factor (VEGF) and inhibited new blood vessel growth in the cornea.
Area of Science:
- Ophthalmology
- Infectious Diseases
- Immunology
Background:
- Pseudomonas aeruginosa ocular infections frequently lead to significant corneal neovascularization.
- Neovascularization, the formation of new blood vessels, can impair vision and compromise corneal health.
Purpose of the Study:
- To investigate the roles of macrophage inflammatory protein-2 (MIP-2) and vascular endothelial growth factor (VEGF) in P. aeruginosa-induced corneal neovascularization.
- To determine if MIP-2 regulates VEGF production during ocular infection.
Main Methods:
- Mice corneas were infected with P. aeruginosa and treated with anti-MIP-2 antibody or control.
- Expression levels of MIP-2 and VEGF were quantified using ELISA.
- Corneal neovascularization was assessed via histology.
- Cellular sources of MIP-2 and VEGF were identified using immunohistochemistry.
Main Results:
- MIP-2 and VEGF expression significantly increased post-infection, correlating with neovascularization.
- Anti-MIP-2 antibody treatment significantly reduced VEGF levels and corneal neovascularization.
- Both corneal resident cells and neutrophils produced MIP-2 and VEGF.
Conclusions:
- MIP-2 and VEGF are key mediators in P. aeruginosa-induced corneal neovascularization.
- MIP-2 plays a regulatory role in the production of VEGF during ocular infection.
