ArticleJournal of cellular and molecular medicine2012
Pro-inflammatory phenotype of COPD fibroblasts not compatible with repair in COPD lung.
Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Next-Generation In Vitro Pulmonary Platforms for Respiratory Disease Modelling and Therapeutic Development: Current Advances and Future Prospects.Medicina (Kaunas, Lithuania) · 2026Review
- Fibroblast-Mediated Macrophage Recruitment Supports Acute Wound Healing.The Journal of investigative dermatology · 2025Article
- Luteal fibroblasts produce prostaglandins in response to IL1β in a MAPK-mediated manner.Molecular and cellular endocrinology · 2025Article
- Deep skin fibroblast-mediated macrophage recruitment supports acute wound healing.bioRxiv : the preprint server for biology · 2024Article
- Altered hypoxia-induced cellular responses and inflammatory profile in lung fibroblasts from COPD patients compared to control subjects.Respiratory research · 2024Article
- Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- DNA nanoparticles targeting FOXO4 selectively eliminate cigarette smoke-induced senescent lung fibroblasts.Nanoscale advances · 2023Article
- Pulmonary inflammation and fibroblast immunoregulation: from bench to bedside.The Journal of clinical investigation · 2023Review
- High-resolution transcriptomic and epigenetic profiling identifies novel regulators of COPD.The EMBO journal · 2023Article
- Evaluation of selected IL6/STAT3 pathway molecules and miRNA expression in chronic obstructive pulmonary disease.Scientific reports · 2021Article
- Article
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- Dexamethasone and p38 MAPK inhibition of cytokine production from human lung fibroblasts.Fundamental & clinical pharmacology · 2021Article
- PAD2-mediated citrullination of Fibulin-5 promotes elastogenesis.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Resident interstitial lung fibroblasts and their role in alveolar stem cell niche development, homeostasis, injury, and regeneration.Stem cells translational medicine · 2021Review
- Article
- The ageing lung under stress.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- E-Liquid Containing a Mixture of Coconut, Vanilla, and Cookie Flavors Causes Cellular Senescence and Dysregulated Repair in Pulmonary Fibroblasts: Implications on Premature Aging.Frontiers in physiology · 2020Article
- Cellular Senescence: The Trojan Horse in Chronic Lung Diseases.American journal of respiratory cell and molecular biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by loss of elastic fibres from small airways and alveolar walls, with the decrease in elastin increasing with disease severity. It is unclear why there is a lack of repair of elastic fibres. We have examined fibroblasts cultured from lung tissue from subjects with or without COPD to determine if the secretory profile explains lack of tissue repair. In this study, fibroblasts were cultured from lung parenchyma of patients with mild COPD [Global initiative for chronic Obstructive Lung Disease (GOLD) 1, n= 5], moderate to severe COPD (GOLD 2-3, n= 12) and controls (non-COPD, n= 5). Measurements were made of proliferation, senescence-associated β-galactosidase-1, mRNA expression of IL-6, IL-8, MMP-1, tropoelastin and versican, and protein levels for IL-6, IL-8, PGE(2,) tropoelastin, insoluble elastin, and versican. GOLD 2-3 fibroblasts proliferated more slowly (P < 0.01), had higher levels of senescence-associated β-galactosidase-1 (P < 0.001) than controls and showed significant increases in mRNA and/or protein for IL-6 (P < 0.05), IL-8 (P < 0.01), MMP-1 (P < 0.05), PGE(2) (P < 0.05), versican (P < 0.05) and tropoelastin (P < 0.05). mRNA expression and/or protein levels of tropoelastin (P < 0.01), versican (P < 0.05), IL-6 (P < 0.05) and IL-8 (P < 0.05) were negatively correlated with FEV1% of predicted. Insoluble elastin was not increased. In summary, fibroblasts from moderate to severe COPD subjects display a secretory phenotype with up-regulation of inflammatory molecules including the matrix proteoglycan versican, and increased soluble, but not insoluble, elastin. Versican inhibits assembly of tropoelastin into insoluble elastin and we conclude that the pro-inflammatory phenotype of COPD fibroblasts is not compatible with repair of elastic fibres.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.