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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2011-3-14
pubmed:abstractText
Recent reports have suggested role for epidermal growth factor receptor (EGFR) in asthma and skin inflammation. Integrin(s) are known to be necessary for the transactivation of EGFR. The roles of EGFR and integrin(s) in allergic inflammation were investigated. Antigen stimulation induced activation of EGFR and interaction between EGFR and integrin ?(5) in Rat Basophilic Leukemia (RBL2H3) cells and bone marrow-derived mouse mast cells (BMMCs). Flow cytometry revealed increased phosphorylation of EGFR on cell surfaces. Antigen stimulation induced interaction between EGFR and Fc?RI in both RBL2H3 cells and BMMCs. Blocking of EGFR or integrin ? exerted negative effects on rac1 activity and secretion of ?-hexosaminidase in both RBL2H3 cells and BMMCs. EGFR and integrin ?(5) were found to be necessary for IgE-dependent cutaneous anaphylaxis. FAK (focal adhesion kinase), interacted with EGFR and with Fc?RI upon antigen stimulation, and it was necessary for the increased secretion of ?-hexosaminidase in both RBL2H3 cells and BMMCs. EGFR and integrin ?(5) were necessary for interactions between activated RBL2H3 cells, BMMCs and rat aortic endothelial cells (RAECs). Conditioned medium of antigen-stimulated RBL2H3 cells promoted RAECs tube formation, rat aortic ring formation and blood vessel formation. Conditioned medium of antigen-stimulated BMMCs also had the same effects on RAECs. This enhanced angiogenic potential of RAECs was dependent on EGFR and integrin ?(5). In conclusion, EGFR, via interaction with Fc?RI and integrin ?(5), is necessary for allergic inflammation associated with cellular interaction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1872-9142
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1035-45
pubmed:meshHeading
pubmed-meshheading:21349584-Animals, pubmed-meshheading:21349584-Asthma, pubmed-meshheading:21349584-Blotting, Western, pubmed-meshheading:21349584-Cell Line, Tumor, pubmed-meshheading:21349584-Cells, Cultured, pubmed-meshheading:21349584-Female, pubmed-meshheading:21349584-Flow Cytometry, pubmed-meshheading:21349584-Focal Adhesion Protein-Tyrosine Kinases, pubmed-meshheading:21349584-Integrin alpha5, pubmed-meshheading:21349584-Male, pubmed-meshheading:21349584-Mast Cells, pubmed-meshheading:21349584-Mice, pubmed-meshheading:21349584-Mice, Inbred BALB C, pubmed-meshheading:21349584-Neovascularization, Physiologic, pubmed-meshheading:21349584-Phosphorylation, pubmed-meshheading:21349584-Protein Binding, pubmed-meshheading:21349584-Rats, pubmed-meshheading:21349584-Rats, Sprague-Dawley, pubmed-meshheading:21349584-Receptor, Epidermal Growth Factor, pubmed-meshheading:21349584-Receptors, IgE, pubmed-meshheading:21349584-Signal Transduction, pubmed-meshheading:21349584-beta-N-Acetylhexosaminidases, pubmed-meshheading:21349584-rac1 GTP-Binding Protein
pubmed:year
2011
pubmed:articleTitle
Integrin ?(5) interacts with EGFR, is necessary for Fc?RI signaling and is necessary for allergic inflammation in relation with angiogenesis.
pubmed:affiliation
Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 200-701, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't