ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Human neutrophil elastase-mediated goblet cell metaplasia is attenuated in TACE-deficient mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting ADAM17 to dampen dendritic cell-mediated type 2 immune responses and airway inflammation associated with allergic asthma.Scientific reports · 2025Article
- Neutrophilic inflammation in bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Neutrophil Elastase and Chronic Lung Disease.Biomolecules · 2021Review
- Endoplasmic reticulum stress/XBP1 promotes airway mucin secretion under the influence of neutrophil elastase.International journal of molecular medicine · 2021Article
- Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Expression and Clinical Significance of Mucin Gene in Chronic Rhinosinusitis.Current allergy and asthma reports · 2020Review
- Targeting Proteases in Cystic Fibrosis Lung Disease. Paradigms, Progress, and Potential.American journal of respiratory and critical care medicine · 2020Review
- Glycosaminoglycans as Multifunctional Anti-Elastase and Anti-Inflammatory Drugs in Cystic Fibrosis Lung Disease.Frontiers in pharmacology · 2020Review
- The EGFR-ADAM17 Axis in Chronic Obstructive Pulmonary Disease and Cystic Fibrosis Lung Pathology.Mediators of inflammation · 2018Review
- Coming to terms with tissue engineering and regenerative medicine in the lung.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Putting the Squeeze on Airway Epithelia.Physiology (Bethesda, Md.) · 2015Review
- Vinpocetine inhibits Streptococcus pneumoniae-induced upregulation of mucin MUC5AC expression via induction of MKP-1 phosphatase in the pathogenesis of otitis media.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophilic inflammation is associated with chronic airway diseases. It has been observed that human neutrophil elastase (HNE), which is secreted by active neutrophils during inflammation, induces both mucin overproduction and goblet cell metaplasia. Several in vitro studies suggest that tumor necrosis factor-α converting enzyme (TACE) regulates the signaling axis that mediates HNE-induced mucin overproduction; however, it is unknown whether TACE performs a similar function in HNE-induced goblet cell metaplasia in vivo. We conducted this study to determine whether the inactivation of Tace gene expression attenuates HNE-induced goblet cell metaplasia in mice. Deletion of Tace is lethal shortly after birth in mice; therefore, we utilized Tace(flox/flox)R26CreER(+/-) mice and induced conditional deletion of Tace using a tamoxifen injection. Wild-type mice were given tamoxifen to control for its effect. Tace conditional deletion mice and wild-type mice were exposed to HNE via nasal instillation three times at 3-day intervals, and the lungs were harvested on day 11 after initial HNE exposure. Using periodic acid-Schiff staining and MUC5AC immunohistochemical staining to visualize goblet cells in the lungs, we found that HNE induced goblet cell metaplasia in the wild-type mice and that HNE-induced goblet cell metaplasia was significantly attenuated in the Tace conditional deletion mice. These findings suggest that TACE could be a potential target in the treatment of goblet cell metaplasia in patients with chronic airway diseases.
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