ArticlePhysiological reports2018
Endoplasmic reticulum, Golgi, and lysosomes are disorganized in lung fibroblasts from chronic obstructive pulmonary disease patients.
Article in Physiological reports, 2018. 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, 35 citations in OpenAlex.
- Spatial and functional characterization of ER stress proteins links fibroblast plasticity and proliferative processes in human osteoarthritic synovitis.Cell death and differentiation · 2026Article
- EWAS in COPD by biomass-burning smoke exposure identifies low levels of endothelin-1 by hypermethylation of EDN1.Epigenomics · 2025Article
- Mechanisms and cross-talk of regulated cell death and their epigenetic modifications in tumor progression.Molecular cancer · 2024Review
- Altered hypoxia-induced cellular responses and inflammatory profile in lung fibroblasts from COPD patients compared to control subjects.Respiratory research · 2024Article
- Expression of Stress-Induced Genes in Bronchoalveolar Lavage Cells and Lung Fibroblasts from Healthy and COPD Subjects.International journal of molecular sciences · 2024Article
- Article
- Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024Review
- Cigarette Smoke Extract Induces MUC5AC Expression Through the ROS/ IP3R/CaInternational journal of chronic obstructive pulmonary disease · 2024Article
- Endoplasmic reticulum stress: a vital process and potential therapeutic target in chronic obstructive pulmonary disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Metabolomics of VToxicology and applied pharmacology · 2023Article
- Effects of hypoxia on bronchial and alveolar epithelial cells linked to pathogenesis in chronic lung disorders.Frontiers in physiology · 2023Article
- Cigarette smoke restricts the ability of mesenchymal cells to support lung epithelial organoid formation.Frontiers in cell and developmental biology · 2023Article
- Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives.Biomolecules · 2022Review
- A Pipeline for Natural Small Molecule Inhibitors of Endoplasmic Reticulum Stress.Frontiers in pharmacology · 2022Article
- Cellular mechanisms involved in the pathogenesis of airway remodeling in chronic lung disease.European clinical respiratory journal · 2022Article
- Diseased lungs may hinder COVID-19 development: A possible reason for the low prevalence of COPD in COVID-19 patients.Medical hypotheses · 2021Article
- Heme oxygenase-1(HO-1) regulates Golgi stress and attenuates endotoxin-induced acute lung injury through hypoxia inducible factor-1α (HIF-1α)/HO-1 signaling pathway.Free radical biology & medicine · 2021Article
- Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles.Autophagy · 2021Review
- The ageing lung under stress.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Endoplasmic reticulum stress and glutathione therapeutics in chronic lung diseases.Redox biology · 2020Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Obstructive Pulmonary Disease (COPD) is often caused by smoking and other stressors. This causes oxidative stress, which induces numerous changes on both the transcriptome and proteome of the cell. We aimed to examine if the endomembrane pathway, including the endoplasmic reticulum (ER), Golgi, and lysosomes, was disrupted in fibroblasts from COPD patients as opposed to healthy ever-smokers or never-smokers, and if the response to stress differed. Different cellular compartments involved in the endomembrane pathway, as well as mRNA expression and apoptosis, were examined before and after the addition of stress in lung fibroblasts from never-smokers, ever-smokers, and patients with COPD. We found that the ER, Golgi, and lysosomes were disorganized in fibroblasts from COPD patients under baseline conditions. After a time course with ER stress inducing chemicals, changes to the phenotypes of cellular compartments in COPD patient fibroblasts were observed, and the expression of the ER stress-induced gene ERP72 was upregulated more in the COPD patient's cells compared to ever-smokers or never-smokers. Lastly, a tendency of increased active Caspase-3 was observed in COPD fibroblasts. Our results show that COPD patients have phenotypic changes in the lung fibroblasts endomembrane pathway, and respond differently to stress. Furthermore, these fibroblasts were cultured for several weeks outside the body, but they were not able to regain proper ER structure, indicating that the internal changes to the endomembrane system are permanent in smokers. This vulnerability to cellular stress might be a cause as to why some smokers develop COPD.
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