ArticleThe American journal of pathology2011
Cigarette smoke-induced pulmonary inflammatory responses are mediated by EGR-1/GGPPS/MAPK signaling.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 58 citations in OpenAlex.
- Timing of dietary effects on the epigenome and their potential protective effects against toxins.Epigenetics · 2025Review
- Metabolic Alterations in Human Post-Mortem Frontal Cortex and Cerebrospinal Fluid Associated With High Levels of Nicotine Metabolite Cotinine.Addiction biology · 2025Article
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- Protective effect of the total alkaloid extract from BulbusFood & nutrition research · 2024Article
- Role of early growth response 1 in inflammation-associated lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Multi-omic association study identifies DNA methylation-mediated genotype and smoking exposure effects on lung function in children living in urban settings.PLoS genetics · 2023Article
- Compound K ameliorates airway inflammation and mucus secretion through the regulation of PKC signaling in vitro and in vivo.Journal of ginseng research · 2022Article
- A Journey into the Clinical Relevance of Heme Oxygenase 1 for Human Inflammatory Disease and Viral Clearance: Why Does It Matter on the COVID-19 Scene?Antioxidants (Basel, Switzerland) · 2022Review
- Potential biomarkers for inflammatory response in acute lung injury.Open medicine (Warsaw, Poland) · 2022Article
- Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells.International journal of molecular sciences · 2019Article
- Overexpression of geranylgeranyl diphosphate synthase contributes to tumour metastasis and correlates with poor prognosis of lung adenocarcinoma.Journal of cellular and molecular medicine · 2018Article
- Recent Advances in the Development of Mammalian Geranylgeranyl Diphosphate Synthase Inhibitors.Molecules (Basel, Switzerland) · 2017Review
- Role of early growth response 1 in liver metabolism and liver cancer.Hepatoma research · 2017Article
- MAPK/FoxA2-mediated cigarette smoke-induced squamous metaplasia of bronchial epithelial cells.International journal of chronic obstructive pulmonary disease · 2017Article
- EGR1 regulates hepatic clock gene amplitude by activating Per1 transcription.Scientific reports · 2015Article
- Lipid-induced Muscle Insulin Resistance Is Mediated by GGPPS via Modulation of the RhoA/Rho Kinase Signaling Pathway.The Journal of biological chemistry · 2015Article
- Hyaluronan fragments as mediators of inflammation in allergic pulmonary disease.Immunobiology · 2015Review
- A systems biology approach reveals the dose- and time-dependent effect of primary human airway epithelium tissue culture after exposure to cigarette smoke in vitro.Bioinformatics and biology insights · 2015Article
- GGPPS1 predicts the biological character of hepatocellular carcinoma in patients with cirrhosis.BMC cancer · 2014Article
- Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early growth response 1 (EGR-1) contributes to the development of chronic obstructive pulmonary disease in the lungs of smokers by mediating pulmonary inflammatory responses, but the direct downstream genes of EGR-1 that regulate this process remain unknown. We show that a new EGR-1 target gene, geranylgeranyl diphosphate synthase (GGPPS), which controls protein prenylation, can regulate the proinflammatory function of EGR-1 by activating MAPK signaling. When C57BL/6 mice were exposed to cigarette smoke, EGR-1 and GGPPS levels increased in their lungs, and the inflammatory responses were augmented, whereas these effects could be reversed by the down-regulation of EGR-1 transcription activity. The accumulation of EGR-1 and GGPPS was induced by MAPK/ERK pathway activation when Beas-2B human bronchial epithelial cells were exposed to cigarette smoke extract (CSE). Further examination showed that EGR-1 in turn regulated Erk1/2 activity because inhibition of EGR-1 transcription activity decreased CSE-induced Erk1/2 phosphorylation. Furthermore, EGR-1-promoted Erk1/2 activation was dependent on GGPPS transcription. Knockdown of GGPPS expression with small-interfering RNA abolished the EGR-1-activated Erk1/2 activity. Both EGR-1 transcription inhibition and GGPPS expression knockdown decreased the inflammatory response induced by CSE in Beas-2B cells. Our results reveal a new EGR-1/GGPPS/MAPK signaling pathway that controls cigarette smoke-induced pulmonary inflammation, and this may shed light on our understanding of the mechanism of cigarette smoke-related pulmonary diseases such as chronic obstructive pulmonary disease.
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