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R.T. Carter, R. Kambampati, C.J. Murphy, E. Bentley; Expression of Matrix Metalloproteinases 2 and 9 in Chronic Wounded Canine Corneas and Spontaneous Chronic Corneal Epithelial Defects (SCCED) . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2157.
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Purpose: Spontaneous chronic corneal epithelial defects (SCCED) are non–healing corneal erosions characterized by redundant, non–adherent epithelium similar to recurrent erosions in humans. Morphology of samples shows sheets of poorly adherent epithelial cells, absence of basement membrane components, and the presence of a superficial hyalinized stromal acellular zone. Matrix metalloproteinases (MMP) remodel the extracellular matrix and are elevated in various pathological processes, including recurrent erosions. Previous work in our lab has shown that expression of MMP 9 is upregulated following acute epithelial wound healing and down–regulated as re–epithelialization is completed in normal dogs; no change is MMP 2 was identified. We evaluated chronic, experimentally wounded corneas and keratectomy samples from SCCED patients for MMP 9 and MMP 2 activity. Methods: Left eyes of 5 normal beagle dogs were used for study. A 10 mm region of the axial cornea underwent mechanical epithelial debridement once a week for 8 weeks. The dogs were humanely euthanized and corneas collected. Superficial keratectomies (n=17) were performed on canine SCCED patients for therapeutic reasons. Samples were homogenized and supernatants collected. Protein concentrations for each sample were obtained to standardize samples. Zymography was performed as previously described. Gels were imaged and statistical analysis was performed to assess for significance. Results: There was no significant difference in values for MMP 9 or MMP2 in chronically wounded corneas versus SCCED samples. Conclusions: Preliminary results show no significant difference in MMP 2 and MMP 9 activity between SCCED and chronically wounded corneas. These data suggest that these MMPs are not involved in the pathophysiology of SCCED and are more likely the response to chronic epithelial injury. These findings emphasize the importance of using a model of chronic wound healing to determine whether changes noted in SCCED patients are due to the underlying pathophysiology or merely due to the presence of a spontaneous chronic corneal epithelial defect.
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