Document Detail


Mast Cell Proteases and Inflammation.
MedLine Citation:
PMID:  22125569     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Mast cells are best known for their role in allergic reactions but are also now recognized for their important contributions to a number of disparate inflammatory conditions through the release of inflammatory mediators, serglycin and other proteoglycans, and proteases. Because these tissue resident inflammatory cells express proteases in such great abundance and their enzymatic activity results in cleavage of a multitude of proteins and peptides, which in turn modify tissue function, their substrate specificity, tissue distribution, and mode of action have become the subjects of great interest. Although mast cell protease-dependent proteolysis is critical to host defense against invading pathogens, regulation of these hydrolytic enzymes is essential to limiting self-induced damage as well. Indeed, dysregulated release of mast cell proteases is now recognized to contribute to the pathogenesis of a number of inflammatory conditions including asthma, abdominal aortic aneurysm formation, vessel damage in atherosclerosis and hypertension, arthritis, and ischemia/reperfusion injury. Understanding how mast cell proteases contribute to inflammation will thus help unravel molecular mechanisms that underlie such immunologic disorders and will help identify new therapeutic targets for drug development.
Authors:
Hongyan Dai; Ronald J Korthuis
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Publication Detail:
Type:  JOURNAL ARTICLE    
Journal Detail:
Title:  Drug discovery today. Disease models     Volume:  8     ISSN:  1740-6757     ISO Abbreviation:  -     Publication Date:  2011  
Date Detail:
Created Date:  2011-11-29     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101235079     Medline TA:  Drug Discov Today Dis Models     Country:  -    
Other Details:
Languages:  ENG     Pagination:  47-55     Citation Subset:  -    
Affiliation:
Department of Medical Pharmacology and Physiology and Dalton Cardiovascular Research Center, University of Missouri, School of Medicine, Columbia, Missouri 65212.
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MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
R01 HL082816-04//NHLBI NIH HHS

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