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dc.contributor.authorAccola, Peter
dc.date.accessioned2014-03-04T18:21:04Z
dc.date.available2014-03-04T18:21:04Z
dc.date.issued2009-12
dc.identifier.otheraccola_peter_j_200912_ms
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/accola_peter_j_200912_ms
dc.identifier.urihttp://hdl.handle.net/10724/25989
dc.description.abstractHeterozygous deficiency in the Pax6 gene results in the analogous condition of aniridia in humans and small eye (Sey) in mice. The underlying pathogenesis is incompletely understood. An in vivo, murine, corneal wounding model was developed to study healing capacity, evaluate the limbal progenitor cell population (p63), and explore the role of soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) in aniridia related keratopathy. Results demonstrated a statistically significant delay in corneal wound healing in Sey mice at days 2 and 3 when compared to WT mice (p<0.05). There was no significant difference in corneal p63 staining (p>0.05). All corneas exhibited comparable sVEGFR-1 staining. In conclusion, our in vivo wounding model revealed delayed corneal healing in Sey mice that does not appear to be due to deficiency in p63 cellular expression. The comparable expression of sVEGFR-1 suggests that it alone is likely not responsible for corneal vascularization present in Sey mice.
dc.languageeng
dc.publisheruga
dc.rightspublic
dc.subjectAniridia related keratopathy
dc.subjectPax6
dc.subjectCornea
dc.subjectAniridia
dc.subjectin vivo
dc.subjectp63
dc.subjectsVEGFR-1
dc.subjectWound
dc.titleEvaluation of corneal healing, limbal progenitor cells, and vascularization in Pax6+/+ and Pax6+/- mice
dc.typeThesis
dc.description.degreeMS
dc.description.departmentVeterinary Pathology
dc.description.majorVeterinary Pathology
dc.description.advisorJames D. Lauderdale
dc.description.advisorK. Paige Carmichael
dc.description.committeeJames D. Lauderdale
dc.description.committeeK. Paige Carmichael
dc.description.committeePhillip A. Moore
dc.description.committeeAngela E. Ellis


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