Document Detail


FGF-10 is decreased in bronchopulmonary dysplasia and suppressed by Toll-like receptor activation.
MedLine Citation:
PMID:  17071719     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Many extremely preterm infants continue to suffer from bronchopulmonary dysplasia, which results from abnormal saccular-stage lung development. Here, we show that fibroblast growth factor-10 (FGF-10) is required for saccular lung development and reduced in the lung tissue of infants with bronchopulmonary dysplasia. Although exposure to bacteria increases the risk of bronchopulmonary dysplasia, no molecular target has been identified connecting inflammatory stimuli and abnormal lung development. In an experimental mouse model of saccular lung development, activation of Toll-like receptor 2 (TLR2) or Toll-like receptor 4 (TLR4) inhibited FGF-10 expression, leading to abnormal saccular airway morphogenesis. In addition, Toll-mediated FGF-10 inhibition disrupted the normal positioning of myofibroblasts around saccular airways, similar to the mislocalization of myofibroblasts seen in patients with bronchopulmonary dysplasia. Reduced FGF-10 expression may therefore link the innate immune system and impaired lung development in bronchopulmonary dysplasia.
Authors:
John T Benjamin; Rebekah J Smith; Brian A Halloran; Timothy J Day; David R Kelly; Lawrence S Prince
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-10-27
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  292     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-02-09     Completed Date:  2007-03-14     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:  L550-8     Citation Subset:  IM    
Affiliation:
Departments of Pediatrics, Children's Hospital of Alabama, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bronchopulmonary Dysplasia / immunology,  metabolism*,  pathology
Disease Models, Animal*
Female
Fetus / drug effects,  pathology
Fibroblast Growth Factor 10 / genetics,  metabolism*
Fibroblasts / drug effects,  pathology
Gene Expression Regulation / drug effects
Humans
Infant, Newborn
Lipopolysaccharides / pharmacology
Lung / drug effects,  pathology
Mice
Mice, Inbred BALB C
RNA, Messenger / genetics,  metabolism
Toll-Like Receptor 2 / metabolism*
Toll-Like Receptor 4 / metabolism*
Transforming Growth Factor beta / metabolism
Chemical
Reg. No./Substance:
0/FGF10 protein, human; 0/Fgf10 protein, mouse; 0/Fibroblast Growth Factor 10; 0/Lipopolysaccharides; 0/RNA, Messenger; 0/Toll-Like Receptor 2; 0/Toll-Like Receptor 4; 0/Transforming Growth Factor beta

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


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