Document Detail

Protection of human corneal epithelial cells from hypoxia-induced disruption of barrier function by hepatocyte growth factor.
MedLine Citation:
PMID:  19944686     Owner:  NLM     Status:  MEDLINE    
The barrier function of the corneal epithelium maintains corneal homeostasis and is mediated by tight junctions (TJs) and adherens junctions (AJs). It is also susceptible to disruption by hypoxia. We have now examined the effects of hypoxia on TJs and AJs as well as on barrier function in human corneal epithelial (HCE) cells. Moreover, we investigated whether such effects of hypoxia might be modulated by hepatocyte growth factor (HGF). The subcellular distribution of the TJ proteins ZO-1 and occludin, the AJ proteins E-cadherin and beta-catenin, and actin filaments was examined by fluorescence microscopy. The abundance of junctional proteins as well as of myosin light chain kinase (MLCK) was determined by immunoblot analysis. Barrier function was evaluated by measurement of transepithelial electrical resistance (TER). Hypoxia-induced both the disappearance of ZO-1 from the borders of neighboring HCE cells as well as the down-regulation of ZO-1 expression without affecting the distribution or abundance of occludin, E-cadherin, or beta-catenin. It also induced the formation of actin stress fibers, the up-regulation of MLCK expression, and a reduction in the TER of HCE cells. All these effects of hypoxia were inhibited by HGF. Neither hypoxia nor HGF exhibited a mitogenic or cytotoxic effect on HCE cells. HGF thus protects HCE cells from hypoxia-induced disruption of barrier function by maintaining the expression and distribution of ZO-1. Inhibition of the effects of hypoxia on the organization of the actin cytoskeleton might also contribute to this protective action of HGF.
Kazuhiro Kimura; Shinichiro Teranishi; Koji Kawamoto; Teruo Nishida
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-11-26
Journal Detail:
Title:  Experimental eye research     Volume:  90     ISSN:  1096-0007     ISO Abbreviation:  Exp. Eye Res.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-15     Completed Date:  2010-03-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370707     Medline TA:  Exp Eye Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  337-43     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Elsevier Ltd. All rights reserved.
Department of Ocular Pathophysiology, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
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MeSH Terms
Adherens Junctions / drug effects*,  metabolism
Anoxia / metabolism*
Biological Transport / drug effects
Cadherins / metabolism
Cell Line, Transformed
Cell Membrane Permeability / drug effects
Cell Proliferation
Electric Impedance
Epithelium, Corneal / drug effects*,  metabolism
Hepatocyte Growth Factor / pharmacology*
Membrane Proteins / metabolism
Microfilaments / metabolism
Microscopy, Fluorescence
Myosin-Light-Chain Kinase / metabolism
Phosphoproteins / metabolism
Tight Junctions / drug effects*,  metabolism
beta Catenin / metabolism
Reg. No./Substance:
0/Cadherins; 0/Membrane Proteins; 0/Phosphoproteins; 0/beta Catenin; 0/occludin; 0/zonula occludens-1 protein; 67256-21-7/Hepatocyte Growth Factor; EC Kinase

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