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J. Yin, F. X. Yu; Impaired Corneal Epithelial Wound Healing, Tear Secretion, and Signal Transduction in Type I Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4786.
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Patients with Diabetes Mellitus (DM) are at an increased risk for developing corneal complications and potential vision loss. The current study uses Type I DM rat model to examine changes in corneal functions, epithelial wound healing, and signal transduction.
Type I DM was induced with streptozotocin (STZ) in male Sprague-Dawley rats. Blood glucose, body weight, body length, corneal diameter, tear secretion, and corneal sensitivity were monitored. Eight weeks after induction of DM, a 5 mm diameter circular corneal epithelial abrasion was created and re-epithelialization was monitored by fluorescein staining and photographed. Signal transduction was evaluated via immunohistochemistry.
STZ-injected rats developed hyperglycemia (>500 mg/dl), while vehicle-injected age-matched controls are normoglycemic (~100 mg/dl). As compared to controls, diabetic rats have significantly decreased body weight and length, slightly smaller corneal diameter, and greatly reduced tear secretion. Eight weeks after DM induction, corneal epithelial wound closure was delayed in DM rats. Wounding resulted in the loss of corneal sensitivity in both diabetic and normal rats; however diabetic rats regained corneal sensitivity post injury more slowly. Diabetic corneas appeared to have altered beta-catenin and occludin distribution, and reduced cell number and cellular intensity of phosphor-AKT in healed epithelia.
DM has profound effects on corneal functions including delayed wound healing, reduced tear secretion, and attenuated sensitivity after injury. Impairment of EGFR-PI3K-AKT signaling in epithelial cells and defect in corneal innervations might be the underlying mechanisms of diabetic corneal disorders.
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