ArticleAmerican journal of respiratory cell and molecular biology2016
DJ-1 Modulates Nuclear Erythroid 2-Related Factor-2-Mediated Protection in Human Primary Alveolar Type II Cells in Smokers.
Article in American journal of respiratory cell and molecular biology, 2016. 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, 38 citations in OpenAlex.
- Inhibition of DJ-1 protects from lupus onset and severity.Scientific reports · 2025Article
- Protective factors against oxidative stress in COPD: focus on Nrf2-dependent antioxidant gene expression.Frontiers in medicine · 2025Review
- Involvement of DJ-1 in the pathogenesis of intervertebral disc degeneration via hexokinase 2-mediated mitophagy.Experimental & molecular medicine · 2024Article
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- DJ-1 is not a deglycase and makes a modest contribution to cellular defense against methylglyoxal damage in neurons.Journal of neurochemistry · 2022Article
- Vaping and Lung Inflammation and Injury.Annual review of physiology · 2022Review
- The role of miRNAs in alveolar epithelial cells in emphysema.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury.Redox biology · 2021Article
- Dysregulated Cell Signaling in Pulmonary Emphysema.Frontiers in medicine · 2021Review
- PARK7 Protects Against Chronic Kidney Injury and Renal Fibrosis by Inducing SOD2 to Reduce Oxidative Stress.Frontiers in immunology · 2021Article
- AITC induces MRP1 expression by protecting against CS/CSE-mediated DJ-1 protein degradationThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- Article
- Inducible expression of heat shock protein 20 protects airway epithelial cells against oxidative injury involving the Nrf2-NQO-1 pathway.Cell & bioscience · 2020Article
- The relationship between DJ-1 and S100A8 in human primary alveolar type II cells in emphysema.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- The role of DJ-1 in human primary alveolar type II cell injury induced by e-cigarette aerosol.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- The effect of cysteine oxidation on DJ-1 cytoprotective function in human alveolar type II cells.Cell death & disease · 2019Article
- Article
- S100A8 Protects Human Primary Alveolar Type II Cells against Injury and Emphysema.American journal of respiratory cell and molecular biology · 2019Article
- Impaired non-homologous end joining in human primary alveolar type II cells in emphysema.Scientific reports · 2019Article
- The cytoprotective role of DJ-1 and p45 NFE2 against human primary alveolar type II cell injury and emphysema.Scientific reports · 2018Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Cigarette smoke (CS) is a main source of oxidative stress and a key risk factor for emphysema, which consists of alveolar wall destruction. Alveolar type (AT) II cells are in the gas exchange regions of the lung. We isolated primary ATII cells from deidentified organ donors whose lungs were not suitable for transplantation. We analyzed the cell injury obtained from nonsmokers, moderate smokers, and heavy smokers. DJ-1 protects cells from oxidative stress and induces nuclear erythroid 2-related factor-2 (Nrf2) expression, which activates the antioxidant defense system. In ATII cells isolated from moderate smokers, we found DJ-1 expression by RT-PCR, and Nrf2 and heme oxygenase (HO)-1 translocation by Western blotting and immunocytofluorescence. In ATII cells isolated from heavy smokers, we detected Nrf2 and HO-1 cytoplasmic localization. Moreover, we found high oxidative stress, as detected by 4-hydroxynonenal (4-HNE) (immunoblotting), inflammation by IL-8 and IL-6 levels by ELISA, and apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay in ATII cells obtained from heavy smokers. Furthermore, we detected early DJ-1 and late Nrf2 expression after ATII cell treatment with CS extract. We also overexpressed DJ-1 by adenovirus construct and found that this restored Nrf2 and HO-1 expression and induced nuclear translocation in heavy smokers. Moreover, DJ-1 overexpression also decreased ATII cell apoptosis caused by CS extract in vitro. Our results indicate that DJ-1 activates the Nrf2-mediated antioxidant defense system. Furthermore, DJ-1 overexpression can restore the impaired Nrf2 pathway, leading to ATII cell protection in heavy smokers. This suggests a potential therapeutic strategy for targeting DJ-1 in CS-related lung diseases.
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