Genetic deletion of Mmp9 does not reduce airway inflammation and structural lung damage in mice with cystic fibrosis-like lung disease
Elevated levels of matrix metalloprotease 9 (MMP-9) and neutrophil elastase (NE) are associated with bronchiectasis and lung function decline in patients with cystic fibrosis (CF). MMP-9 is a potent extracellular matrix-degrading enzyme which is activated by NE and has been implicated in structural...
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| Hauptverfasser: | , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2 November 2022
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| In: |
International journal of molecular sciences
Year: 2022, Jahrgang: 23, Heft: 21, Pages: 1-13 |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms232113405 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3390/ijms232113405 Verlag, lizenzpflichtig, Volltext: https://www.mdpi.com/1422-0067/23/21/13405 
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| Verfasserangaben: | Claudius Wagner, Anita Balázs, Jolanthe Schatterny, Zhe Zhou-Suckow, Julia Duerr, Carsten Schultz and Marcus A. Mall |
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| 245 | 1 | 0 | |a Genetic deletion of Mmp9 does not reduce airway inflammation and structural lung damage in mice with cystic fibrosis-like lung disease |c Claudius Wagner, Anita Balázs, Jolanthe Schatterny, Zhe Zhou-Suckow, Julia Duerr, Carsten Schultz and Marcus A. Mall |
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| 520 | |a Elevated levels of matrix metalloprotease 9 (MMP-9) and neutrophil elastase (NE) are associated with bronchiectasis and lung function decline in patients with cystic fibrosis (CF). MMP-9 is a potent extracellular matrix-degrading enzyme which is activated by NE and has been implicated in structural lung damage in CF. However, the role of MMP-9 in the in vivo pathogenesis of CF lung disease is not well understood. Therefore, we used β-epithelial Na+ channel-overexpressing transgenic (βENaC-Tg) mice as a model of CF-like lung disease and determined the effect of genetic deletion of Mmp9 (Mmp9-/-) on key aspects of the pulmonary phenotype. We found that MMP-9 levels were elevated in the lungs of βENaC-Tg mice compared with wild-type littermates. Deletion of Mmp9 had no effect on spontaneous mortality, inflammatory markers in bronchoalveolar lavage, goblet cell metaplasia, mucus hypersecretion and emphysema-like structural lung damage, while it partially reduced mucus obstruction in βENaC-Tg mice. Further, lack of Mmp9 had no effect on increased inspiratory capacity and increased lung compliance in βENaC-Tg mice, whereas both lung function parameters were improved with genetic deletion of NE. We conclude that MMP-9 does not play a major role in the in vivo pathogenesis of CF-like lung disease in mice. | ||
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| 650 | 4 | |a lung damage | |
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| 650 | 4 | |a neutrophil elastase | |
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