Document Detail

Biosynthesized matrix provides a key role for survival signaling in bronchial epithelial cells.
MedLine Citation:
PMID:  14617518     Owner:  NLM     Status:  MEDLINE    
The extracellular matrix (ECM) influences a variety of cellular functions, including survival, adhesion molecule expression, differentiation, and migration. The ECM composition of the epithelial basement membrane is altered in asthmatics. In this study, we elucidate the major survival signals received by bronchial epithelial cells in vitro by studying the effects of a variety of ECM factors and soluble growth factors on bronchial epithelial cell survival. Our findings indicate that the insulin family of soluble growth factors provides important survival signals but also that adhesion to ECM is a crucial determinant of bronchial epithelial cell survival. In the BEAS-2B bronchial epithelial cell line, collagens I and IV, laminin, fibronectin, and vitronectin provide significant levels of protection from apoptosis. Tenascin-C has no effect, whereas elastin and collagen V increase apoptosis to above control levels. BEAS-2B cells secrete their own biosynthesized matrix (BSM), which also provides rescue from apoptosis. Protection by collagen I, fibronectin, and vitronectin was found to be via an RGD domain. Laminin-, collagen IV-, and BSM-mediated survival is not RGD dependent. Primary bronchial epithelial cells exhibit a similar pattern of apoptosis rescue to the BEAS-2B cell line, although we did not observe any vitronectin-mediated protection in the primary cells. These data indicate that bronchial epithelial cell survival is dependent both on soluble growth factors and on a variety of ECM-derived signals.
Sam J Wadsworth; Anette M Freyer; Randolph L Corteling; Ian P Hall
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-11-14
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  286     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-02-05     Completed Date:  2004-03-26     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L596-603     Citation Subset:  IM    
Division of Therapeutics and Molecular Medicine, South Block, D Floor, University Hospital, Nottingham NG7 2UH, United Kingdom.
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MeSH Terms
Apoptosis / drug effects,  physiology*
Basement Membrane / physiology
Blood Proteins / pharmacology
Bronchi / cytology*
Cell Line, Transformed
Cell Survival / drug effects,  physiology
Extracellular Matrix / physiology
Extracellular Matrix Proteins / pharmacology
Growth Substances / pharmacology
Respiratory Mucosa / cytology*
Signal Transduction / drug effects,  physiology*
Reg. No./Substance:
0/Blood Proteins; 0/Extracellular Matrix Proteins; 0/Growth Substances

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

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