ArticleAmerican journal of respiratory cell and molecular biology2007
Cigarette smoke stimulates matrix metalloproteinase-2 activity via EGR-1 in human lung fibroblasts.
Article in American journal of respiratory cell and molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics.Cell communication and signaling : CCS · 2023Pooled it
- Network Pharmacology and Experimental Verification Reveal the Regulatory Mechanism of Chuanbeimu in Treating Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
- The evaluation of the MMP-2/TIMP-1 ratio in peptic ulcer and its association with refractory helicobacter pylori infection.BMC gastroenterology · 2023Article
- Role of early growth response 1 in inflammation-associated lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- The role of cancer stromal fibroblasts in mediating the effects of tobacco-induced cancer cell growth.Cancer cell international · 2021Review
- Unravelling the Network of Nuclear Matrix Metalloproteinases for Targeted Drug Design.Biology · 2020Review
- Mir-29b mediates the regulation of Nrf2 on airway epithelial remodeling and Th1/Th2 differentiation in COPD rats.Saudi journal of biological sciences · 2019Article
- The ex vivo human lung: research value for translational science.JCI insight · 2019Review
- Pentagalloyl glucose increases elastin deposition, decreases reactive oxygen species and matrix metalloproteinase activity in pulmonary fibroblasts under inflammatory conditions.Biochemical and biophysical research communications · 2018Article
- Cigarette smoke reversibly activates hypoxia-inducible factor 1 in a reactive oxygen species-dependent manner.Scientific reports · 2016Article
- Matrix Remodeling in Pulmonary Fibrosis and Emphysema.American journal of respiratory cell and molecular biology · 2016Review
- Article
- Egr-1: new conductor for the tissue repair orchestra directs harmony (regeneration) or cacophony (fibrosis).The Journal of pathology · 2013Review
- The role of Src kinase in macrophage-mediated inflammatory responses.Mediators of inflammation · 2012Review
- Smoking and idiopathic pulmonary fibrosis.Pulmonary medicine · 2012Article
- GGPPS, a new EGR-1 target gene, reactivates ERK 1/2 signaling through increasing Ras prenylation.The American journal of pathology · 2011Article
- Cigarette smoke-induced pulmonary inflammatory responses are mediated by EGR-1/GGPPS/MAPK signaling.The American journal of pathology · 2011Article
- c-Jun regulates shear- and injury-inducible Egr-1 expression, vein graft stenosis after autologous end-to-side transplantation in rabbits, and intimal hyperplasia in human saphenous veins.The Journal of biological chemistry · 2010Article
- Matrix metalloproteinase-14 mediates a phenotypic shift in the airways to increase mucin production.American journal of respiratory and critical care medicine · 2009Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Recent reports of increased matrix metalloproteinase-2 (MMP-2) in lungs of patients with emphysema support the paradigm of proteinase/antiproteinase imbalance in the pathogenesis of COPD. We sought to define the signaling pathways activated by smoke and to identify molecules responsible for emphysema-associated MMP-2 expression. In this study, we show that cigarette smoke extract (CSE) induced MMP-2 protein expression and increased MMP-2 gelatinase activity of normal lung fibroblasts. We previously identified a transcription factor, early growth response 1 (EGR-1), with robust expression in the lung tissues of patients with COPD compared with control smokers. Here, the treatment of fibroblasts with CSE resulted in marked induction of EGR-1 mRNA and protein in a dose- and time-dependent manner, accompanied by increased EGR-1 binding activity. CSE-induced MMP-2 mRNA and protein expression and activity were significantly inhibited using EGR-1 small interfering RNA (siRNA) or in Egr-1-null(-/-) mouse fibroblasts. Furthermore, we observed induction of membrane type 1 matrix metalloproteinase (MT1-MMP), which has an EGR-1-binding site on its promoter, in CSE-treated primary normal lung fibroblasts. The concomitant MT1-MMP expression and MMP-2 activation by CSE are inhibited by EGR-1 siRNA. Rapid activation of mitogen-activated protein kinases was observed in CSE-treated fibroblasts. Chemical inhibitors of ERK1/2 MAPK, but not of p38 and JNK, decreased CSE-induced EGR-1 protein expression and MMP-2 activity of fibroblasts. The identification that induction of MMP-2 and MT1-MMP by CSE from lung fibroblasts is EGR-1-dependent reveals a molecular mechanism for matrix remodeling in cigarette smoke-related emphysema.
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Registered trials
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