Document Detail


The Rac1/JNK pathway is critical for EGFR-dependent barrier formation in human airway epithelial cells.
MedLine Citation:
PMID:  21036915     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The airway epithelial barrier provides defenses against inhaled antigens and pathogens, and alterations of epithelial barrier function have been proposed to play a significant role in the pathogenesis of chronic airway diseases. Although the epidermal growth factor receptor (EGFR) plays roles in various physiological and pathological processes on the airway epithelium, the role of EGFR on barrier function in the airway remains largely unknown. In the present study, we assessed the effects of EGFR activation on paracellular permeability in airway epithelial cells (AECs). EGFR activation induced by the addition of EGF increased transepithelial electrical resistance (TER) in AECs. An EGFR-blocking antibody eradicated the development of TER, paracellular influx of dextran, and spatial organization of tight junction. Moreover, the effects of EGFR activation on paracellular permeability were eradicated by knockdown of occludin. To identify the EGFR signaling pathway that regulates permeability barrier development, we investigated the effects of several MAP kinase inhibitors on permeability barrier function. Pretreatment with a JNK-specific inhibitor, but not an ERK- or p38-specific inhibitor, attenuated the development of TER induced by EGFR activation. Rac1 is one of the upstream activators for JNK in EGFR signaling. Rac1 knockdown attenuated the phosphorylation of JNK activation and EGFR-mediated TER development. These results suggest that EGFR positively regulates permeability barrier development through the Rac1/JNK-dependent pathway.
Authors:
Masahiro Terakado; Yasuhiro Gon; Akiko Sekiyama; Ikuko Takeshita; Yutaka Kozu; Ken Matsumoto; Noriaki Takahashi; Shu Hashimoto
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-29
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  300     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-20     Completed Date:  2011-01-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L56-63     Citation Subset:  IM    
Affiliation:
Dept. of Internal Medicine, Nihon Univ. School of Medicine, Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
Airway Obstruction / physiopathology*
Cell Membrane Permeability / drug effects,  physiology
Epidermal Growth Factor / pharmacology
Epithelial Cells / drug effects,  physiology*
Humans
Lung / physiology*
MAP Kinase Kinase 4 / metabolism*
MAP Kinase Signaling System / physiology*
Mitogen-Activated Protein Kinases / metabolism
Receptor, Epidermal Growth Factor / drug effects,  immunology,  physiology*
Tight Junctions / drug effects,  physiology
rac1 GTP-Binding Protein / physiology*
Chemical
Reg. No./Substance:
62229-50-9/Epidermal Growth Factor; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.12.2/MAP Kinase Kinase 4; EC 3.6.5.2/rac1 GTP-Binding Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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