ArticleCommunicative & integrative biology2011
Specific ion fluxes generate cornea wound electric currents.
Article in Communicative & integrative biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Measurement of Anions in Dog Tear Fluid Using Ion Chromatography.Veterinary ophthalmology · 2026Article
- Caveolin-1-mediated STAT3 activation determines electrotaxis of human lung cancer cells.Oncotarget · 2017Article
- Diabetic cornea wounds produce significantly weaker electric signals that may contribute to impaired healing.Scientific reports · 2016Article
- Physiological controls of large-scale patterning in planarian regeneration: a molecular and computational perspective on growth and form.Regeneration (Oxford, England) · 2016Article
- Cannabinoid-induced chemotaxis in bovine corneal epithelial cells.Investigative ophthalmology & visual science · 2015Article
- Molecular bioelectricity: how endogenous voltage potentials control cell behavior and instruct pattern regulation in vivo.Molecular biology of the cell · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The corneal epithelium generates a significant trans-epithelial potential (TEP) which aids in maintaining cornea water balance and transparency. Injury to the cornea causes a short circuit of the TEP at the wound. The TEP in the intact epithelium around the wound acts like a battery, powering significant ion flux and electric current at the wound. These circulating endogenous currents generate an electric field orientated towards the wound, with the wound the cathode. Many cell types, including human corneal epithelial cells and keratinocytes, migrate to the cathode at physiological electric field strengths. Indeed, the electric signal is a powerful stimulator of cell migration, which appears to override other cues such as chemotaxis and wound void. These wound fields also have a dynamic timecourse of change after wounding. It has been assumed that wound electric fields are produced by passive leakage of ions from damaged cells and tissue. Could these fields be actively maintained and regulated as an active wound response? What are the molecular, ionic and cellular mechanisms underlying the wound electric currents?
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Registered trials
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