Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 295: C378-C387, 2008. First published May 21, 2008; doi:10.1152/ajpcell.90624.2007
0363-6143/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
295/2/C378    most recent
90624.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Yin, J.
Right arrow Articles by Yu, F.-S. X.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yin, J.
Right arrow Articles by Yu, F.-S. X.

PROTEIN AND VESICLE TRAFFICKING, CYTOSKELETON

Rho kinases regulate corneal epithelial wound healing

Jia Yin and Fu-Shin X. Yu

Departments of Ophthalmology, Anatomy and Cell Biology, Kresge Eye Institute, Wayne State University School of Medicine, Detroit, Michigan

Submitted 13 December 2007 ; accepted in final form 15 May 2008

We have previously shown that Rho small GTPase is required for modulating both cell migration and proliferation through cytoskeleton reorganization and focal adhesion formation in response to wounding. In the present study, we investigated the role of Rho kinases (ROCKs), major effectors of Rho GTPase, in mediating corneal epithelial wound healing. Both ROCK 1 and 2 were expressed and activated in THCE cells, an SV40-immortalized human corneal epithelial cell (HCEC) line, in response to wounding, lysophosphatidic acid, and heparin-binding EGF-like growth factor (HB-EGF) stimulations. The ROCK inhibitor Y-27632 efficiently antagonized ROCK activities without affecting Rho activation in wounded HCECs. Y-27632 promoted basal and HB-EGF-enhanced scratch wound healing and enhanced cell migration and adhesion to matrices, while retarded HB-EGF induced cell proliferation. E-cadherin- and β-catenin-mediated cell-cell junction and actin cytoskeleton organization were disrupted by Y-27632. Y-27632 impaired the formation and maintenance of tight junction barriers indicated by decreased trans-epithelial resistance and disrupted occludin staining. We conclude that ROCK activities enhance cell proliferation, promote epithelial differentiation, but negatively modulate cell migration and cell adhesion and therefore play a role in regulating corneal epithelial wound healing.

corneal epithelial cells; cell migration; cell proliferation; cell-matrix adhesion; cell-cell junctions



Address for reprint requests and other correspondence: F.-S X. Yu, Kresge Eye Institute, Wayne State Univ. School of Medicine, 4717 St. Antoine Blvd, Detroit, MI, 48201 (e-mail: fyu{at}med.wayne.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.