Journal article
Extracellular matrix proteoglycan degradation by human alveolar macrophages and neutrophils
Journal of applied physiology (1985), Vol.66(1), pp.400-409
01/1989
DOI: 10.1152/jappl.1989.66.1.400
PMID: 2917944
Abstract
Degradation and restructuring of the elastin fiber network of the lung is a pivotal process in the pathogenesis of emphysema. Alveolar macrophages and neutrophils are probably directly involved in elastin degradation, but they may also indirectly influence elastin structure and function by altering other extracellular matrix components such as proteoglycans. In this study the mechanisms of proteoglycan degradation by human alveolar macrophages and neutrophils have been explored. Macrophages appear to utilize plasminogen in solubilizing 35SO4-labeled proteoglycans in extracellular matrix produced by neonatal rat vascular smooth muscle cells. Proteoglycan degradation by macrophages is significantly augmented in the presence of 1% human serum. In contrast, neutrophils apparently utilize intrinsic proteinases to solubilize extracellular matrix proteoglycans, and serum inhibits proteoglycan degradation by these cells. Persistent inflammation in the terminal airways of cigarette smokers may produce proteoglycan degradation and influence elastin fiber architecture where the earliest physiological and anatomic evidence of emphysema appears.
Details
- Title: Subtitle
- Extracellular matrix proteoglycan degradation by human alveolar macrophages and neutrophils
- Creators
- Stephen E McGowan - Department of Internal Medicine, University of Iowa College of Medicine, Iowa CityRhinda J Thompson - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Journal of applied physiology (1985), Vol.66(1), pp.400-409
- DOI
- 10.1152/jappl.1989.66.1.400
- PMID
- 2917944
- NLM abbreviation
- J Appl Physiol (1985)
- ISSN
- 8750-7587
- eISSN
- 1522-1601
- Publisher
- United States
- Language
- English
- Date published
- 01/1989
- Academic Unit
- International Programs; Internal Medicine
- Record Identifier
- 9983984536302771
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