Abstract

Corneal disease is a major problem in both wild and captive pinnipeds. In recent years, several studies have shown that eye diseases are one of the main problems seen in pinnipeds in the wild and in captivity, yet it is unclear why pinnipeds have a higher occurrence of ocular disease than other marine mammals.^2-5,7 While there are many contributing environmental factors in captive settings, such as water quality and UV light,^3,5 it is proposed that the frequency of pinniped ocular disease is due in part to either inadequacy or absence of the neovascularization response necessary for corneal wound healing.⁶ This study is the first to examine the presence or absence of vascularization and the angiogenic pathway components, vascular endothelial growth factor (VEGF) and VEGF-receptor-2 (VEGFR-2), in pinniped corneas. We hypothesize that pinnipeds possess the functional components of this neovascularization pathway, but the pathway is not being adequately triggered in response to injury due to some other factor(s). Tissue sections from 41 pinniped globes were stained immunohistochemically using goat polyclonal anti-VEGF and anti-VEGFR-2 antibodies. Canine globes were used as controls, as dogs are closely related terrestrial relatives to pinnipeds and have a known, effective corneal neovascularization response.¹ Trained, blind observers used light microscopy to visualize the stained slides to qualitatively evaluate the presence of vascular tissue and grade the intensity of the reaction. The results show positive expression of VEGF and VEGFR-2 in both normal and diseased pinniped corneas. In diseased corneas, the intensity of the reaction was less than the canine controls for both VEGF and VEGFR-2. These results suggest that pinnipeds do possess the functional components of the neovascularization pathway, but perhaps another factor in the cornea that moderates this process is absent or insufficient. The next step is to investigate such factors that act as chaperones to VEGF and neovascularization. This will provide valuable insight into the neovascularization capabilities in the pinniped eye, which could lead to a better understanding of why pinniped ocular disease occurs so frequently, and eventually how to better treat and prevent ocular disease in both captive and rehabilitation settings.

Acknowledgements

Research supported by the Merial Veterinary Scholars Program, The Medway Scholarship from the International Association for Aquatic Animal Medicine, and the Florida Fish and Wildlife Conservation Commission. The authors would like to thank Pat Lewis for her technical assistance and the Dubielzig Lab for providing specimens.

* Presenting author
⁺ Student presenter

Literature Cited

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