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Verfasst von:Wagner, Claudius [VerfasserIn]   i
 Balázs, Anita [VerfasserIn]   i
 Schatterny, Jolanthe [VerfasserIn]   i
 Zhou-Suckow, Zhe [VerfasserIn]   i
 Duerr, Julia [VerfasserIn]   i
 Schultz, Carsten [VerfasserIn]   i
 Mall, Marcus A. [VerfasserIn]   i
Titel:Genetic deletion of Mmp9 does not reduce airway inflammation and structural lung damage in mice with cystic fibrosis-like lung disease
Verf.angabe:Claudius Wagner, Anita Balázs, Jolanthe Schatterny, Zhe Zhou-Suckow, Julia Duerr, Carsten Schultz and Marcus A. Mall
E-Jahr:2022
Jahr:2 November 2022
Umfang:13 S.
Fussnoten:Gesehen am 23.01.2023
Titel Quelle:Enthalten in: International journal of molecular sciences
Ort Quelle:Basel : Molecular Diversity Preservation International, 2000
Jahr Quelle:2022
Band/Heft Quelle:23(2022), 21, Artikel-ID 13405, Seite 1-13
ISSN Quelle:1422-0067
 1661-6596
Abstract: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.
DOI:doi:10.3390/ijms232113405
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.3390/ijms232113405
 Volltext: https://www.mdpi.com/1422-0067/23/21/13405
 DOI: https://doi.org/10.3390/ijms232113405
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:airway inflammation
 lung damage
 matrix metalloproteinase 9
 neutrophil elastase
K10plus-PPN:1831770016
Verknüpfungen:→ Zeitschrift

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