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Detection of Functional Matrix Metalloproteinases by Zymography
Published on: November 8, 2010
Matrix metalloproteinases in emphysema
Sina A Gharib1, Anne M Manicone1, William C Parks2
1Center for Lung Biology, University of Washington, Seattle, WA, USA.
Abstract:
Several studies have implicated a causative role for specific matrix metalloproteinases (MMPs) in the development and progression of cigarette smoke-induced chronic obstructive pulmonary disease (COPD) and its severe sequela, emphysema. However, the precise function of any given MMP in emphysema remains an unanswered question. Emphysema results from the degradation of alveolar elastin - among other possible mechanisms - a process that is often thought to be caused by elastolytic proteinases made by macrophages. In this article, we discuss the data suggesting, supporting, or refuting causative roles of macrophage-derived MMPs, with a focus on MMPs-7, -9, -10, -12, and 28, in both the human disease and mouse models of emphysema. Findings from experimental models suggest that some MMPs, such as MMP-12, may directly breakdown elastin, whereas others, particularly MMP-10 and MMP-28, promote the development of emphysema by influencing the proteolytic and inflammatory activities of macrophages.
Insights
Matrix metalloproteinases (MMPs) are implicated in chronic obstructive pulmonary disease (COPD) and emphysema. Some MMPs directly degrade elastin, while others influence macrophage activity to promote emphysema development.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Immunology
Background:
- Cigarette smoke-induced chronic obstructive pulmonary disease (COPD) and emphysema are linked to matrix metalloproteinases (MMPs).
- The specific roles of individual MMPs in emphysema pathogenesis remain unclear.
- Emphysema involves alveolar elastin degradation, potentially by macrophage-derived elastolytic proteinases.
Purpose of the Study:
- To review and discuss evidence for the causative roles of specific macrophage-derived MMPs in emphysema.
- To focus on MMP-7, -9, -10, -12, and -28 in human disease and mouse models.
Main Methods:
- Review of existing scientific literature and experimental data.
- Analysis of findings from human studies and mouse models of emphysema.
- Focus on the functions of specific matrix metalloproteinases (MMPs) derived from macrophages.
Main Results:
- Experimental models suggest MMP-12 may directly degrade elastin.
- MMP-10 and MMP-28 appear to promote emphysema by modulating macrophage proteolytic and inflammatory functions.
- Evidence for the roles of MMP-7 and MMP-9 is also considered.
Conclusions:
- Specific matrix metalloproteinases (MMPs) play distinct roles in the development of emphysema.
- MMP-12 directly contributes to elastin degradation.
- MMP-10 and MMP-28 influence macrophage behavior, exacerbating emphysema progression.
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