Document Detail

Increased sensitivity of asthmatic airway smooth muscle cells to prostaglandin E2 might be mediated by increased numbers of E-prostanoid receptors.
MedLine Citation:
PMID:  15131569     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: An increase in airway smooth muscle (ASM) cell proliferation leads to an increase in the bulk of the ASM, one of the characteristic features of asthma. We have previously shown that ASM cells from asthmatic individuals proliferate more than those from nonasthmatic subjects. This increased growth might be due to compromised inhibitory mechanisms within the ASM of asthmatic subjects. OBJECTIVE: The purpose of this study was to determine whether the proliferative control exerted by prostaglandin E(2) (PGE(2)) was altered in the asthmatic ASM cells. METHODS: We used tritated thymidine uptake to measure cell proliferation and cell-surface ELISAs to detect the presence of cell-surface receptors on ASM cells isolated from asthmatic and nonasthmatic individuals. RESULTS: The asthmatic ASM cells were significantly more sensitive to proliferation inhibition by PGE(2) than the nonasthmatic cells (P<.02). The PGE(2) (E-prostanoid [EP]) receptors EP2 and EP3 were detected on asthmatic and nonasthmatic smooth muscle cells in culture. There were significantly more receptors on the asthmatic cells. The asthmatic cells also had increased sensitivity to proliferation inhibition by EP2-specific agonists but not by EP3-specific agonists. CONCLUSION: The increased growth observed in asthmatic ASM cells is not the result of impaired responsiveness to PGE(2). In contrast, these cells have increased sensitivity. This increased sensitivity might be mediated by the increased numbers of EP2 receptors on the surface.
Janette K Burgess; Qi Ge; Sarah Boustany; Judith L Black; Peter R A Johnson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  113     ISSN:  0091-6749     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-05-07     Completed Date:  2004-06-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  876-81     Citation Subset:  AIM; IM    
Respiratory Research Group, Department of Pharmacology, Bosch Building D05, University of Sydney, Sydney, NSW 2006, Australia.
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MeSH Terms
Asthma / metabolism*,  pathology*
Cell Division / drug effects
Cells, Cultured
Dinoprostone / pharmacology*
Epoprostenol / pharmacology
Forskolin / pharmacology
Lung / drug effects,  metabolism,  pathology
Muscle, Smooth / drug effects*,  metabolism,  pathology
Receptors, Prostaglandin E / agonists,  metabolism*
Reg. No./Substance:
0/Receptors, Prostaglandin E; 0/prostaglandin EP2 receptor; 0/prostaglandin EP3 receptor; 35121-78-9/Epoprostenol; 363-24-6/Dinoprostone; 66428-89-5/Forskolin

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