Matrix metalloproteinase expression and production by alveolar macrophages in emphysema.

@article{Finlay1997MatrixME,
  title={Matrix metalloproteinase expression and production by alveolar macrophages in emphysema.},
  author={G A Finlay and L. R. O’Driscoll and K. J. Russell and E M D'arcy and James B. Masterson and Muiris X. FitzGerald and Clare M. O'connor},
  journal={American journal of respiratory and critical care medicine},
  year={1997},
  volume={156 1},
  pages={
          240-7
        }
}
The aim of this study was to examine the hypothesis that alveolar macrophages represent a significant source of matrix-degrading proteinases in the emphysematous lung. Macrophages from bronchoalveolar lavage fluid of 10 patients with emphysema and 10 normal volunteers were maintained in vitro for 24 h and assessed semiquantitatively for mRNA transcript levels of the matrix metalloproteinases (MMPs) gelatinases A and B, macrophage metalloelastase (MME), and interstitial collagenase. Release of… 

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References

SHOWING 1-10 OF 34 REFERENCES

Elastin degradation by human alveolar macrophages. A prominent role of metalloproteinase activity.

A prominent role for metalloproteinase activity in elastin degradation by both human and murine macrophages is indicated and support the concept that events at the cell-substrate interface are critically important to macrophage-mediated elast in degradation.

Alveolar macrophage modulation of proteolysis by neutrophil elastase in extracellular matrix.

It is suggested that AM can release previously internalized NE in an enzymatically active form and that AM may enhance collagen degradation in matrix that was also exposed to NE.

Neutral metalloproteinases produced by human mononuclear phagocytes. Enzyme profile, regulation, and expression during cellular development.

The potential of macrophages to directly degrade extracellular matrix via secreted metalloproteinases in a manner that differs both qualitatively and quantitatively from that of fibroblasts is confirmed.

Elastolytic metalloproteinases produced by human mononuclear phagocytes. Potential roles in destructive lung disease.

  • S. Shapiro
  • Biology
    American journal of respiratory and critical care medicine
  • 1994
The most newly described member of the MMP family is human macrophage metalloelastase, a major product of human alveolar macrophages that is also an elastase.

Alveolar inflammation and its relation to emphysema in smokers.

The data suggest that as long as the inflammatory reaction is predominantly of neutrophils there is no destruction of the lung, and the extent of lung destruction becomes evident, and its extent is directly related to the number of alveolar macrophages and T-lymphocytes/mm3.

Excessive neutrophil elastase in bronchoalveolar lavage fluid in subclinical emphysema.

It is concluded that NE-alpha 1-PI complex in BALF is a factor that may differentiate smokers who are potentially developing emphysema from those who are not, and NE inhibitory activity measured by a spectrophotometric method did not show any significant difference between the two groups of current smokers.

The role of thiol proteases in tissue injury and remodeling.

Human lung macrophages express all four of the known lysosomal thiol proteases and recent studies of the differential expression of these cathepsins suggest they not only cooperate in terminal degradation of endocytized protein but also have specific functions such as proenzyme activation, antigen processing, and tissue remodeling, especially bone matrix resorption.

Degradation of connective tissue matrices by macrophages. III. Morphological and biochemical studies on extracellular, pericellular, and intracellular events in matrix proteolysis by macrophages in culture

Extracellular, pericellular, and lysosomal events each contribute to degradation of extracellular matrix macromolecules by inflammatory macrophages.

Elastin and collagen remodeling in emphysema. A scanning electron microscopy study.

The novel concept of increased collagen deposition and aberrant collagen remodeling in the pathogenesis of emphysema is supported by ultrastructural examination of elastin and collagen templates in an animal model of empysema and in human lungs.