ArticleAmerican journal of respiratory and critical care medicine2009
Matrix metalloproteinase-14 mediates a phenotypic shift in the airways to increase mucin production.
Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 49 citations in OpenAlex.
- Bulb ofJournal of microbiology and biotechnology · 2023Article
- Review
- Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2023Review
- Effects of Wood Smoke Constituents on Mucin Gene Expression in Mice and Human Airway Epithelial Cells and on Nasal Epithelia of Subjects with a Susceptibility Gene Variant inEnvironmental health perspectives · 2022Article
- The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD.Respiratory research · 2021Review
- Phloretin, an Apple Polyphenol, Inhibits Pathogen-Induced Mucin Overproduction.Molecular nutrition & food research · 2021Article
- Interferon-γ enhances the antifibrotic effects of pirfenidone by attenuating IPF lung fibroblast activation and differentiation.Respiratory research · 2019Article
- Acute cardiopulmonary toxicity of inhaled aldehydes: role of TRPA1.Annals of the New York Academy of Sciences · 2016Review
- Neurovascular remodeling in the aged ischemic brain.Journal of neural transmission (Vienna, Austria : 1996) · 2015Review
- SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation.Acta histochemica et cytochemica · 2015Article
- COPD: balancing oxidants and antioxidants.International journal of chronic obstructive pulmonary disease · 2015Review
- Novel proteolytic microvesicles released from human macrophages after exposure to tobacco smoke.The American journal of pathology · 2013Article
- Mechanistic links between COPD and lung cancer.Nature reviews. Cancer · 2013Review
- Article
- MT1-MMP cooperates with Kras(G12D) to promote pancreatic fibrosis through increased TGF-β signaling.Molecular cancer research : MCR · 2011Article
- Role of aberrant metalloproteinase activity in the pro-inflammatory phenotype of bronchial epithelium in COPD.Respiratory research · 2011Article
- Haplotype association mapping of acute lung injury in mice implicates activin a receptor, type 1.American journal of respiratory and critical care medicine · 2011Article
- Review
- Endothelial dysfunction and claudin 5 regulation during acrolein-induced lung injury.American journal of respiratory cell and molecular biology · 2011Article
- Quercetin prevents progression of disease in elastase/LPS-exposed mice by negatively regulating MMP expression.Respiratory research · 2010Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleInduced mainly by cigarette smoking, chronic obstructive pulmonary disease (COPD) is a global public health problem characterized by progressive difficulty in breathing and increased mucin production. Previously, we reported that acrolein levels found in COPD sputum could activate matrix metalloproteinase-9 (MMP9).
objectivesTo determine whether acrolein increases expression and activity of MMP14, a critical membrane-bound endopeptidase that can initial a MMP-activation cascade.
methodsMMP14 activity and adduct formation were measured following direct acrolein treatment. MMP14 expression and activity was measured in human airway epithelial cells. MMP14 immunohistochemistry was performed with COPD tissue, and in acrolein- or tobacco-exposed mice. MEASUREMENTS AND MAIN
resultsIn a cell-free system, acrolein, in concentrations equal to those found in COPD sputum, directly adducted cysteine 319 in the MMP14 hemopexin-like domain and activated MMP14. In cells, acrolein increased MMP14 activity, which was inhibited by a proprotein convertase inhibitor, hexa-d-arginine. In the airway epithelium of COPD subjects, immunoreactive MMP14 protein increased. In mouse lung, acrolein or tobacco smoke increased lung MMP14 activity and protein. In cells, acrolein-induced MMP14 transcripts were inhibited by an epidermal growth factor receptor (EGFR) neutralizing antibody, EGFR kinase inhibitor, metalloproteinase inhibitor, or mitogen-activated protein kinase (MAPK) 3/2 or MAPK8 inhibitors, but not a MAPK14 inhibitor. Decreasing the MMP14 protein and activity in vitro by small interfering (si)RNA to MMP14 diminished the acrolein-induced MUC5AC transcripts. In acrolein-exposed mice or transgenic mice with lung-specific transforming growth factor-alpha (an EGFR ligand) expression, lung MMP14 and MUC5AC levels increased and these effects were inhibited by a EGFR inhibitor, erlotinib.
conclusionsTaken together, these findings implicate acrolein-induced MMP14 expression and activity in mucin production in COPD.
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