ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
Cigarette smoke-induced expression of heme oxygenase-1 in human lung fibroblasts is regulated by intracellular glutathione.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 89 citations in OpenAlex.
- Exercise and smoking: health rivals revealing shared protective mechanisms in Parkinson's?NPJ Parkinson's disease · 2026Review
- Iron metabolism dysregulation and ferroptosis: Emerging drivers in pulmonary fibrosis pathogenesis and therapy.Molecules and cells · 2025Review
- Comparative Evaluation of Cigarette Smoke and a Heated Tobacco Product on Corneal Oxidative Stress in an Air/Liquid Interface Model.Investigative ophthalmology & visual science · 2025Article
- N‑acetyl‑L‑cysteine protects rat lungs and RLE‑6TN cells from cigarette smoke‑induced oxidative stress.Molecular medicine reports · 2025Article
- Identifying polymorphic cis-regulatory variants as risk markers for lung carcinogenesis and chemotherapy responses in tobacco smokers from eastern India.Scientific reports · 2023Article
- Dietary Antioxidants and Lung Cancer Risk in Smokers and Non-Smokers.Healthcare (Basel, Switzerland) · 2022Review
- Ninjinyoeito ameliorated cigarette smoke extract-induced apoptosis and inflammation through JNK signaling inhibition in human lung fibroblasts.BMC complementary medicine and therapies · 2022Article
- Standardized Cannabis Smoke Extract Induces Inflammation in Human Lung Fibroblasts.Frontiers in pharmacology · 2022Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Angiotensin-converting enzyme 2 expression in COPD and IPF fibroblasts: the forgotten cell in COVID-19.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- COVID-19 and heme oxygenase: novel insight into the disease and potential therapies.Cell stress & chaperones · 2020Review
- Suppressing endoplasmic reticulum stress-related autophagy attenuates retinal light injury.Aging · 2020Article
- Risuteganib Protects against Hydroquinone-induced Injury in Human RPE Cells.Investigative ophthalmology & visual science · 2020Article
- Cigarette smoke increases susceptibility to infection in lung epithelial cells by upregulating caveolin-dependent endocytosis.PloS one · 2020Article
- Comparison of in vitro toxicological effects of biomass smoke from different sources of animal dung.Toxicology in vitro : an international journal published in association with BIBRA · 2017Article
- Article
- Dung biomass smoke activates inflammatory signaling pathways in human small airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Predicting the Cytotoxic Potency of Cigarette Smoke by Assessing the Thioredoxin Reductase Inhibitory Capacity of Cigarette Smoke Extract.International journal of environmental research and public health · 2016Article
- The Role of Mitochondria and Oxidative/Antioxidative Imbalance in Pathobiology of Chronic Obstructive Pulmonary Disease.Oxidative medicine and cellular longevity · 2016Review
- Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression.Respiratory research · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblasts are key structural cells that can be damaged by cigarette smoke. Cigarette smoke contains many components capable of eliciting oxidative stress, which may induce heme oxygenase (HO)-1, a cytoprotective enzyme. There are no data on HO-1 expression in primary human lung fibroblasts after cigarette smoke extract (CSE) exposure. We hypothesized that human lung fibroblasts exposed to cigarette smoke would increase HO-1 though changes in intracellular glutathione (GSH). Primary human lung fibroblasts were exposed to CSE, and changes in HO-1 expression and GSH levels were assessed. CSE induced a time- and dose-dependent increase in expression of HO-1, but not HO-2 or biliverdin reductase, in two different primary human lung fibroblast strains, a novel finding. This induction of HO-1 paralleled a decrease in intracellular GSH, and a sustained reduction in GSH resulted in a dramatic increase in HO-1. Treatment with the antioxidants N-acetyl-l-cysteine or GSH reduced the expression of HO-1 induced by CSE. We also examined the signal transduction mechanism responsible for HO-1 induction. Nuclear factor erythroid-derived 2, like 2 (Nrf2) was not involved in HO-1 induction by CSE. Activator protein-1 (AP-1) is a redox-sensitive transcription factor shown in other systems to regulate HO-1 expression. CSE exposure resulted in nuclear accumulation of c-Fos and c-Jun, two key AP-1 components. Reduction of c-Fos and c-Jun nuclear translocation by SP-600125 attenuated the CSE-induced expression of HO-1. These data support the concept that changes in the cellular redox status brought on by cigarette smoke induce HO-1 in fibroblasts. This increase in HO-1 may help protect against cigarette smoke-induced inflammation and/or cell death.
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