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HGF, MAPK, and a small physiological electric field interact during corneal epithelial cell migration
Vikki A McBain1, John V Forrester, Colin D McCaig
1Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen, Scotland, United Kingdom. vikkimcbain@breathemail.net
Investigative Ophthalmology & Visual Science
|January 31, 2003
Summary
Hepatocyte growth factor (HGF) and electric fields (EF) significantly increase corneal epithelial cell (CEC) migration rate by activating MAPK signaling. EF also causes receptor redistribution, potentially aiding migration maintenance.
Area of Science:
- Ophthalmology
- Cell Biology
- Biophysics
Background:
- Corneal epithelial cell (CEC) migration is crucial for wound healing.
- Hepatocyte growth factor (HGF) is known to promote cell migration.
- The role of electric fields (EFs) in modulating cell migration is an area of active research.
Purpose of the Study:
- To investigate the combined effects of HGF and EF on CEC migration.
- To elucidate the underlying molecular mechanisms, including receptor localization and signaling pathway activation.
Main Methods:
- Primary bovine CEC cultures were treated with HGF and/or EF.
- CEC migration rate and directionality were quantified.
- Expression and localization of HGF receptors (HGFRs) and MAPK pathway activation were analyzed using confocal microscopy and Western blotting.
Main Results:
- Both HGF and EF significantly enhanced CEC migration rate.
- EF induced an asymmetrical distribution of HGFRs towards the cathode.
- HGF and EF activated the MAPK signaling pathway, with greater activation on the cathode side in the presence of EF.
Conclusions:
- HGF and EF accelerate CEC migration by activating the p42/44 MAPK pathway.
- EF-induced HGFR redistribution and MAPK asymmetry may play roles in migration signaling and maintenance, though not directly directing migration.
- These findings offer insights into therapeutic strategies for corneal wound healing.