April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Injury Induced Expression Of Chloride Channels Contributes To Corneal Wound Electric Currents
Author Affiliations & Notes
  • Min Zhao
    Dermatology and Ophthalmology,
    University of California Davis, Davis, California
  • Brian Reid
    Dermatology & Ophthalmology,
    University of California Davis, Davis, California
  • Lin Cao
    Dermatology & Ophthalmology, UC Davis & University of Aberdeen, Davis, California
  • Tsung-Yu Chen
    University of California Davis, Davis, California
  • Xiaodong Zhang
    Dermatology and Ophthalmology,
    University of California Davis, Davis, California
  • Footnotes
    Commercial Relationships  Min Zhao, None; Brian Reid, None; Lin Cao, None; Tsung-Yu Chen, None; Xiaodong Zhang, None
  • Footnotes
    Support  NIH 1R01EY019101. Also 1R01GM065447, CIRM RB1-01417, NSF MCB-0951199
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2019. doi:
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      Min Zhao, Brian Reid, Lin Cao, Tsung-Yu Chen, Xiaodong Zhang; Injury Induced Expression Of Chloride Channels Contributes To Corneal Wound Electric Currents. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2019.

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

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Purpose: : The corneal epithelium has multiple functions including mechanical protection from pathogens and refraction of light onto the lens and retina. The integrity of the epithelial surface is necessary for normal vision. Fortunately most corneal epithelial wounds are repaired promptly. Wounding the corneal epithelium, and many other epithelia, results in production of large electric currents and fields at the wound which stimulate epithelial cell division and migration into the wound bed to initiate and promote healing. These endogenous wound currents appears to be actively-regulated and we have shown that enhancing or inhibiting the wound currents pharmacologically can increase or decrease wound healing, respectively. Using ion-selective microelectrodes, we have shown that chloride is the major ion generating the wound electric currents, with lesser contributions by calcium and sodium. The purpose of this study was to identify the ion channels and pumps responsible. By defining the electrophysiological properties of the cornea, we will be able to understand the mechanisms of endogenous wound electric current generation, and offer new approaches to manage corneal injury and/or disease.

Methods: : We examined the expression and distribution of Cl- channels in cornea wounds using quantitative PCR, Western blot and immunohistochemistry. Patch clamp with flash induced photorelease of calcium and ion selective probe were used to determine the Cl- currents in corneal epithelial cells. Using a vibrating probe system we measured cornea wound electric currents in ex vivo eyes in the presence of various ion channel blockers.

Results: : Wounding induced significant changes in expression profiles of Cl- channels. We found Ca2+ dependent Cl- currents in corneal epithelial cells. Broad-spectrum chloride channel blocker DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate) significantly reduced (almost halved) cornea wound current (P<0.003). Fluoxetine hydrochloride, which blocks calcium-dependent chloride current, reduced wound current slightly. Interestingly, mefloquine hydrochloride reversed the small outward current normally seen in unwounded cornea to produce an inward current (P<0.03). Injury to the cornea caused significant re-distribution and increased expression of ion channels near the wound.

Conclusions: : Injury induced changes in expression profile of Cl- channels in corneal epithelium contribute to cornea wound electric currents.

Keywords: cornea: epithelium • ion transporters • ion channels 

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