Corneal Complications in Streptozocin-Induced Type I Diabetic Rats
Open Access
- 1 August 2011
- journal article
- cornea
- Published by Association for Research in Vision and Ophthalmology (ARVO) in Investigative Ophthalmology & Visual Science
- Vol. 52 (9), 6589-6596
- https://doi.org/10.1167/iovs.11-7709
Abstract
Purpose.: This study seeks to characterize corneal functions and complications in a streptozocin (STZ)-induced rat model of type I diabetes mellitus (DM) and to understand the pathogenesis of diabetic keratopathy. Methods.: DM was induced via STZ injection in Sprague-Dawley rats. Body weight, length, and corneal size were measured and compared with the age-matched normal controls. Corneal morphology and histology were evaluated with slit lamp, digital confocal microscopy and hematoxylin and eosin staining. Tear secretion was measured with cotton threads, and corneal sensitivity was determined with an esthesiometer. Protein expression and distribution were assessed with Western blotting and immunohistochemistry. Wound healing was determined using an in vivo corneal epithelial debridement model. Results.: Compared with the normal control rats, STZ rats had reduced body weight, and body length, but minimally affected corneal size. No significant changes in ocular surface regularity, corneal thickness, and morphology were noted in diabetic corneas. STZ rats showed stronger Rose Bengal staining, decreased tear secretion, slightly attenuated sensitivity, less innervation, delayed epithelial wound healing, and impaired epidermal growth factor receptor signaling in their corneas. While the expression of adherens junction protein β-catenin, and tight junction proteins occludin and ZO-1 was unchanged, the formation of these junctions after wound closure was delayed. Conclusions.: Pathogenesis of diabetic keratopathy involves multiple tissues and/or cell types and several events including reduced tear secretion, impaired innervation, weakened cell junction, and altered wound responses. These insights may prove useful for the clinical translation of evolving strategies for the management and treatment of diabetic corneal complications.This publication has 59 references indexed in Scilit:
- Impaired Epithelial Wound Healing and EGFR Signaling Pathways in the Corneas of Diabetic RatsInvestigative Ophthalmology & Visual Science, 2011
- LL-37 via EGFR Transactivation to Promote High Glucose–Attenuated Epithelial Wound Healing in Organ-Cultured CorneasInvestigative Ophthalmology & Visual Science, 2010
- High Glucose Suppresses Epidermal Growth Factor Receptor/Phosphatidylinositol 3-Kinase/Akt Signaling Pathway and Attenuates Corneal Epithelial Wound HealingDiabetes, 2009
- ERK1/2 Mediate Wounding- and G-protein-Coupled Receptor Ligands-Induced EGFR Activation via Regulating ADAM17 and HB-EGF SheddingInvestigative Ophthalmology & Visual Science, 2009
- Corneal Subbasal Nerve Density: A Comparison of Two Confocal MicroscopesEye & Contact Lens: Science & Clinical Practice, 2008
- Rho kinases regulate corneal epithelial wound healingAmerican Journal of Physiology-Cell Physiology, 2008
- Naltrexone accelerates healing without compromise of adhesion complexes in normal and diabetic corneal epitheliumBrain Research Bulletin, 2007
- Wound-induced ATP release and EGF receptor activation in epithelial cellsJournal of Cell Science, 2007
- Lysophosphatidic Acid Promoting Corneal Epithelial Wound Healing by Transactivation of Epidermal Growth Factor ReceptorInvestigative Ophthalmology & Visual Science, 2007
- Src-Family Tyrosine Kinases in Wound- and Ligand-Induced Epidermal Growth Factor Receptor Activation in Human Corneal Epithelial CellsInvestigative Ophthalmology & Visual Science, 2006