Document Detail


Interleukin-1beta augments in vitro alveolar epithelial repair.
MedLine Citation:
PMID:  11076808     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Biologically active interleukin (IL)-1beta is present in the pulmonary edema fluid obtained from patients with acute lung injury and has been implicated as an important early mediator of nonpulmonary epithelial wound repair. Therefore, we tested the hypothesis that IL-1beta would enhance wound repair in cultured monolayers from rat alveolar epithelial type II cells. IL-1beta (20 ng/ml) increased the rate of in vitro alveolar epithelial repair by 118 +/- 11% compared with that in serum-free medium control cells (P < 0.01). IL-1beta induced cell spreading and migration at the edge of the wound but not proliferation. Neutralizing antibodies to epidermal growth factor (EGF) and transforming growth factor-alpha or inhibition of the EGF receptor by tyrphostin AG-1478 or genistein inhibited IL-1beta-induced alveolar epithelial repair, indicating that IL-1beta enhances in vitro alveolar epithelial repair by an EGF- or transforming growth factor-alpha-dependent mechanism. Moreover, the mitogen-activated protein kinase pathway is involved in IL-1beta-induced alveolar epithelial repair because inhibition of extracellular signal-regulated kinase activation by PD-98059 inhibited IL-1beta-induced alveolar epithelial repair. In conclusion, IL-1beta augments in vitro alveolar epithelial repair, indicating a possible novel role for IL-1beta in the early repair process of the alveolar epithelium in acute lung injury.
Authors:
T Geiser; P H Jarreau; K Atabai; M A Matthay
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  279     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2000 Dec 
Date Detail:
Created Date:  2000-12-01     Completed Date:  2000-12-22     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  L1184-90     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130, USA. thomas.geiser@insel.ch
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MeSH Terms
Descriptor/Qualifier:
Animals
Enzyme Inhibitors / pharmacology
Epidermal Growth Factor / pharmacology
Epithelial Cells / drug effects,  enzymology
Flavonoids / pharmacology
Interleukin-1 / pharmacology*
MAP Kinase Signaling System / physiology
Male
Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism
Pulmonary Alveoli / cytology*
Rats
Rats, Sprague-Dawley
Receptor, Epidermal Growth Factor / antagonists & inhibitors
Respiratory Distress Syndrome, Adult / pathology
Respiratory Mucosa / drug effects*,  physiology*
Specific Pathogen-Free Organisms
Transforming Growth Factor alpha / pharmacology
Wound Healing / drug effects
Grant Support
ID/Acronym/Agency:
HL-51854/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0/Enzyme Inhibitors; 0/Flavonoids; 0/Interleukin-1; 0/Transforming Growth Factor alpha; 62229-50-9/Epidermal Growth Factor; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.11.24/Mitogen-Activated Protein Kinases

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


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