ArticleAmerican journal of respiratory cell and molecular biology2008
Acrolein-activated matrix metalloproteinase 9 contributes to persistent mucin production.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 119 citations in OpenAlex.
- An aberrant leukotriene A4 hydrolase-proline-glycine-proline pathway in the pathogenesis of chronic obstructive pulmonary disease.American journal of respiratory and critical care medicine · 2014Trial
- Epithelial cells in chronic obstructive pulmonary disease exacerbations: Targets for lung repair.Pharmacological reviews · 2026Review
- Effects of Aerosol Extract From Heated Tobacco Products on Senescence-Associated Gene Expression in Human Lung Fibroblasts.Geriatrics & gerontology international · 2026Article
- E-cigarette aerosols of propylene glycol impair BK channel activity and parameters of mucociliary function.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Review
- Review
- Mucus Hypersecretion in Chronic Obstructive Pulmonary Disease and Its Treatment.Mediators of inflammation · 2023Review
- Phloretin, an Apple Polyphenol, Inhibits Pathogen-Induced Mucin Overproduction.Molecular nutrition & food research · 2021Article
- Dual Substance Use of Electronic Cigarettes and Alcohol.Frontiers in physiology · 2020Review
- Analysis of Acrolein Exposure Induced Pulmonary Response in Seven Inbred Mouse Strains and Human Primary Bronchial Epithelial Cells Cultured at Air-Liquid Interface.BioMed research international · 2020Article
- Bronchial epithelium repair by Esculentin-1a-derived antimicrobial peptides: involvement of metalloproteinase-9 and interleukin-8, and evaluation of peptides' immunogenicity.Scientific reports · 2019Article
- Alternative Oxidase Attenuates Cigarette Smoke-induced Lung Dysfunction and Tissue Damage.American journal of respiratory cell and molecular biology · 2019Article
- CD147 increases mucus secretion induced by cigarette smoke in COPD.BMC pulmonary medicine · 2019Article
- The relationship between acrolein and oxidative stress in COPD: in systemic plasma and in local lung tissue.International journal of chronic obstructive pulmonary disease · 2019Article
- E-Cigarette Use Causes a Unique Innate Immune Response in the Lung, Involving Increased Neutrophilic Activation and Altered Mucin Secretion.American journal of respiratory and critical care medicine · 2018Article
- Proteomic identification of moesin upon exposure to acrolein.Proteome science · 2018Article
- Positive feedback of the amphiregulin-EGFR-ERK pathway mediates PM2.5 from wood smoke-induced MUC5AC expression in epithelial cells.Scientific reports · 2017Article
- Inhibitors of ceramide de novo biosynthesis rescue damages induced by cigarette smoke in airways epithelia.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- The Contribution of Small Airway Obstruction to the Pathogenesis of Chronic Obstructive Pulmonary Disease.Physiological reviews · 2017Review
- A Potential Role for Acrolein in Neutrophil-Mediated Chronic Inflammation.Inflammation · 2015Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD), a global public health problem, is characterized by progressive difficulty in breathing, with increased mucin production, especially in the small airways. Acrolein, a constituent of cigarette smoke and an endogenous mediator of oxidative stress, increases airway mucin 5, subtypes A and C (MUC5AC) production; however, the mechanism remains unclear. In this study, increased mMUC5AC transcripts and protein were associated with increased lung matrix metalloproteinase 9 (mMMP9) transcripts, protein, and activity in acrolein-exposed mice. Increased mMUC5AC transcripts and mucin protein were diminished in gene-targeted Mmp9 mice [Mmp9((-/-))] or in mice treated with an epidermal growth factor receptor (EGFR) inhibitor, erlotinib. Acrolein also decreased mTissue inhibitor of metalloproteinase protein 3 (an MMP9 inhibitor) transcript levels. In a cell-free system, acrolein increased pro-hMMP9 cleavage and activity in concentrations (100-300 nM) found in sputum from subjects with COPD. Acrolein increased hMMP9 transcripts in human airway cells, which was inhibited by an MMP inhibitor, EGFR-neutralizing antibody, or a mitogen-activated protein kinase (MAPK) 3/2 inhibitor. Together these findings indicate that acrolein can initiate cleavage of pro-hMMP9 and EGFR/MAPK signaling that leads to additional MMP9 formation. Augmentation of hMMP9 activity, in turn, could contribute to persistent excessive mucin production.
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