EC Number   |
General Information |
Reference |
|---|
   3.4.24.65 | malfunction |
degradation of elastin is central to the pathogenesis of emphysema |
709415 |
| 3.4.24.65 | malfunction |
MMP12 is implicated in inflammatory respiratory disorders such as asthma, pulmonary fibrosis and chronic obstructive pulmonary disease, with a critical role of MMP12 in the development of emphysema. MMP inhibitors applied in animal models of emphysema are successful in reducing lung inflammation |
709559 |
| 3.4.24.65 | malfunction |
Streptococcus pneumoniae infection aggravates elastase-induced emphysema, with increased mortality and an increased number of inflammatory cells in bronchoalveolar lavage fluid, via matrix metalloproteinase 12 overexpression, also resulting in enhanced emphysema progression. The increased MMP-12 production is mostly due to alveolar type II cells, alveolar macrophages, and lymphocytes that aggregate around vessels and bronchioles. Dexamethasone treatment suppresses the mortality rate and number of inflammatory cells in bronchoalveolar lavage fluid but not emphysema progression, possibly owing to the failure of MMP-12 suppression in the lungs, whereas treatment with the MMP inhibitor ONO-4817 dramatically suppressea both mortality rate and emphysema progression |
-, 754337 |
| 3.4.24.65 | metabolism |
neutrophil elastase (NE) and matrix metalloproteinase 12 (MMP12) activity is increased at the surface of bronchoalveolar neutrophils and macrophages and is associated with structural lung damage in betaENaC-Tg mice |
754734 |
| 3.4.24.65 | physiological function |
HME is able to degrade extracellular matrix components such as elastin and is involved in tissue remodeling processes. Overexpression of HME is strongly correlated with the reduced angiogenesis and vascular invasion of gastric carcinoma |
708303 |
| 3.4.24.65 | physiological function |
in MMP-12 deficient mice, deficiency has no significant effect on total body weight or on subcutaneous or gonadal adipose tissue mass. Adipocyte and blood vessel size and density in subcutaneous and gonadal adipose tissues of obese mice are also comparable in MMP-12 deficient and control mice. Macrophage infiltration in subcutaneous and gonadal adipose tissues is not affected by MMP-12 deficiency, but the amount of crown-like structures is significantly lower. MMP-12 deficiency does not affect elastin content in the extracellular matrix of subcutaneous or gonadal adipose tissue |
733392 |
| 3.4.24.65 | physiological function |
macrophage elastase (matrix metalloproteinase 12, MMP12) is an additional protease contributing to early lung damage in betaENaC-overexpressing (betaENaC-Tg) mice, suffering cystic fibrosis (CF)-like lung disease, besides neutrophil elastatse (EC 3.4.21.37). MMP12 contributes to structural lung damage in mice with CF-like lung disease |
754734 |
| 3.4.24.65 | physiological function |
macrophage elastase is able to degrade extracellular matrix components such as elastin and is involved in tissue remodeling in inflammatory respiratory diseases such as chronic obstructive pulmonary diseases, including emphysema. MMP-12 is also involved in asthma and fibrosis. Inhibitors demonstrate a reduction in both the inflammatory process and airspace enlargement in lung tissue. MMP-12 plays a predominant role in the inflammatory process induced by cigarette smoke |
708452 |
| 3.4.24.65 | physiological function |
macrophage elastase is able to degrade extracellular matrix components such as elastin and is involved in tissue remodeling in inflammatory respiratory diseases such as chronic obstructive pulmonary diseases, including emphysema. MMP-12 is involved in fibrosis, mechanism, overview. Balb/c mice are resistant to the development of pulmonary fibrosis, while C57BL/6 mice are not, overview |
708452 |
| 3.4.24.65 | physiological function |
macrophage elastase, or MMP-12, is mainly produced by alveolar macrophages and is believed to play a major role in the development of chronic obstructive pulmonary disease (COPD). MMP-12 is predominantly produced by activated macrophages at sites of inflammation. MMP-12 seems to also have a function in regulating antiviral immunity. The protease may enter the nucleus of a virus-infected cell where it serves as a transcription factor driving the transcription of the IkappaBalpha gene. This results in the secretion of the antiviral molecule interferon-alpha. The second, distinct role of MMP-12 in antiviral immunity is to proteolytically clear interferon-alpha from the blood, so allowing the virus-induced inflammation to be resolved |
752886 |
