Document Detail


The role of electrical signals in murine corneal wound re-epithelialization.
MedLine Citation:
PMID:  20945376     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ion flow from intact tissue into epithelial wound sites results in lateral electric currents that may represent a major driver of wound healing cell migration. Use of applied electric fields (EF) to promote wound healing is the basis of Medicare-approved electric stimulation therapy. This study investigated the roles for EFs in wound re-epithelialization, using the Pax6(+/-) mouse model of the human ocular surface abnormality aniridic keratopathy (in which wound healing and corneal epithelial cell migration are disrupted). Both wild-type (WT) and Pax6(+/-) corneal epithelial cells showed increased migration speeds in response to applied EFs in vitro. However, only Pax6(+/+) cells demonstrated consistent directional galvanotaxis towards the cathode, with activation of pSrc signaling, polarized to the leading edges of cells. In vivo, the epithelial wound site normally represents a cathode, but 43% of Pax6(+/-) corneas exhibited reversed endogenous wound-induced currents (the wound was an anode). These corneas healed at the same rate as WT. Surprisingly, epithelial migration did not correlate with direction or magnitude of endogenous currents for WT or mutant corneas. Furthermore, during healing in vivo, no polarization of pSrc was observed. We found little evidence that Src-dependent mechanisms of cell migration, observed in response to applied EFs in vitro, normally exist in vivo. It is concluded that endogenous EFs do not drive long-term directionality of sustained healing migration in this mouse corneal epithelial model. Ion flow from wounds may nevertheless represent an important component of wound signaling initiation.
Authors:
Romana Kucerova; Petr Walczysko; Brian Reid; Jingxing Ou; Lucy J Leiper; Ann M Rajnicek; Colin D McCaig; Min Zhao; J Martin Collinson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  226     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-03-17     Completed Date:  2011-05-16     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1544-53     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Wiley-Liss, Inc.
Affiliation:
School of Medical Sciences, Institute of Medical Sciences Foresterhill, University of Aberdeen, Aberdeen AB25 2ZD, UK.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Cell Movement
Electricity*
Enzyme Activation
Epithelial Cells / enzymology,  pathology
Epithelium, Corneal / enzymology,  injuries*,  pathology*
Eye Proteins / metabolism
Homeodomain Proteins / metabolism
Humans
Immunohistochemistry
Mice
Paired Box Transcription Factors / metabolism
Protein Transport
Repressor Proteins / metabolism
Time Factors
Wound Healing*
src-Family Kinases / metabolism
Grant Support
ID/Acronym/Agency:
068012//Wellcome Trust; 1R01EY019101/EY/NEI NIH HHS; BB/E015840/1//Biotechnology and Biological Sciences Research Council; R01 EY019101/EY/NEI NIH HHS; R01 EY019101-01A2/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Eye Proteins; 0/Homeodomain Proteins; 0/PAX6 protein; 0/Paired Box Transcription Factors; 0/Repressor Proteins; EC 2.7.10.2/src-Family Kinases
Comments/Corrections

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