April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
Impaired Corneal Epithelial Wound Healing, Tear Secretion, and Signal Transduction in Type I Diabetic Rats
Author Affiliations & Notes
  • J. Yin
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • F. X. Yu
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • Footnotes
    Commercial Relationships  J. Yin, None; F.X. Yu, None.
  • Footnotes
    Support  NIH Grant EY10869 and EY17960 (F.X. Yu); Alliance for Vision Research (J.Y.)
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4786. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      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.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements

Purpose: : 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.

Methods: : 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.

Results: : 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.

Conclusions: : 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.

Keywords: cornea: epithelium • wound healing • diabetes 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.