Document Detail


Mast cell chymase modifies cell-matrix interactions and inhibits mitogen-induced proliferation of human airway smooth muscle cells.
MedLine Citation:
PMID:  12097409     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The hallmarks of chronic, severe asthma include prominent airway inflammation and airway smooth muscle (ASM) hypertrophy and hyperplasia. One of the factors that contribute to the injury and repair process within the airway is activation of proteases and turnover of extracellular matrix components. Mast cells, which are present in increased numbers in the asthmatic airway, are a rich source of the neutral protease chymase, which can degrade several basement membrane components. Recent data suggest that proteases also play a critical role in regulating the expression of CD44, the primary receptor for the matrix glycosaminoglycan hyaluronan. In this study we investigated the effects of chymase treatment on human ASM cell function. We found that chymase degraded the smooth muscle cell pericellular matrix. This was accompanied by an increased release of fibronectin and soluble CD44, but not soluble ICAM-1 or soluble hyaluronan, into the conditioned medium. In addition, chymase inhibited T cell adhesion to ASM and dramatically reduced epidermal growth factor-induced smooth muscle cell proliferation. These data suggest that the local release of mast cell chymase may have profound effects on ASM cell function and airway remodeling.
Authors:
Aili L Lazaar; Michael I Plotnick; Umberto Kucich; Irene Crichton; Shidan Lotfi; Susan K P Das; Sibyl Kane; Joel Rosenbloom; Reynold A Panettieri; Norman M Schechter; Ellen Puré
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  169     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-07-04     Completed Date:  2002-08-28     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1014-20     Citation Subset:  AIM; IM    
Affiliation:
Pulmonary, Allergy and Critical Care Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. alazaar@mail.med.upenn.edu
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MeSH Terms
Descriptor/Qualifier:
Antigens, CD44 / metabolism
Cell Adhesion / physiology
Cell Communication / physiology*
Cells, Cultured
Chymases
Down-Regulation
Epidermal Growth Factor / pharmacology
Extracellular Matrix / enzymology,  metabolism*,  pathology
Growth Inhibitors / pharmacology,  physiology*
Humans
Mast Cells / enzymology*
Mitogens / antagonists & inhibitors,  pharmacology*
Muscle, Smooth / cytology,  enzymology*
Serine Endopeptidases / pharmacology,  physiology*
Signal Transduction / physiology
Solubility
Trachea / cytology,  enzymology*
Grant Support
ID/Acronym/Agency:
AI45813/AI/NIAID NIH HHS; AR42931/AR/NIAMS NIH HHS; HL55301/HL/NHLBI NIH HHS; HL56401/HL/NHLBI NIH HHS; HL64042/HL/NHLBI NIH HHS; HL64063/HL/NHLBI NIH HHS; HL67663/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD44; 0/Growth Inhibitors; 0/Mitogens; 62229-50-9/Epidermal Growth Factor; EC 3.4.21.-/Serine Endopeptidases; EC 3.4.21.39/Chymases

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