ArticlePloS one2011
Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.
Article in PloS one, 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, 68 citations in OpenAlex.
- HSP60 and SARS-CoV-2: Les Liaisons Dangereuses.Biology · 2025Review
- Role of Regulatory T Cells in Pulmonary Ageing and COPD Development.International journal of molecular sciences · 2025Review
- Lung Single-Cell Transcriptomics Offers Insights into the Pulmonary Interstitial Toxicity Caused by Silica Nanoparticles.Environment & health (Washington, D.C.) · 2024Article
- Review
- Exosome regulation of immune response mechanism: Pros and cons in immunotherapy.Bioactive materials · 2024Article
- Mitochondrial damage-associated molecular patterns in chronic obstructive pulmonary disease: Pathogenetic mechanism and therapeutic target.Journal of translational internal medicine · 2023Article
- Fractional heat shock protein 27 urine excretion as a short-term predictor in acute exacerbation of chronic obstructive pulmonary disease.Annals of translational medicine · 2021Article
- The ageing lung under stress.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Role of HSP60/HSP10 in Lung Cancer: Simple Biomarkers or Leading Actors?Journal of oncology · 2020Review
- Novel serum markers HSP60, CHI3L1, and IGFBP-2 in metastatic colorectal cancer.Oncology letters · 2019Article
- Hsp60 as a Novel Target in IBD Management: A Prospect.Frontiers in pharmacology · 2019Review
- Toward Developing Chemical Modulators of Hsp60 as Potential Therapeutics.Frontiers in molecular biosciences · 2018Review
- HSP60 activity on human bronchial epithelial cells.International journal of immunopathology and pharmacology · 2017Article
- Serum Heat Shock Protein Levels and the Relationship of Heat Shock Proteins with Various Parameters in Chronic Obstructive Pulmonary Disease Patients.Turkish thoracic journal · 2016Article
- COPD immunopathology.Seminars in immunopathology · 2016Review
- The histone deacetylase inhibitor SAHA induces HSP60 nitration and its extracellular release by exosomal vesicles in human lung-derived carcinoma cells.Oncotarget · 2016Article
- Response to: Hsp27 and Hsp70 in chronic obstructive pulmonary disease.Cell stress & chaperones · 2015Article
- Hsp27 and Hsp70 in chronic obstructive pulmonary disease: certainties vs doubts.Cell stress & chaperones · 2015Article
- Hsp10 nuclear localization and changes in lung cells response to cigarette smoke suggest novel roles for this chaperonin.Open biology · 2014Article
- Innate immunity but not NLRP3 inflammasome activation correlates with severity of stable COPD.Thorax · 2014Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses. METHODS AND
resultsBronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between the number of neutrophils and Hsp60 levels. Double-immunostaining showed that Hsp60-positive neutrophils were significantly increased in COPD patients. We then investigated in vitro the effect on Hsp60 expression in bronchial epithelial cells (16HBE) caused by oxidative stress, a hallmark of COPD mucosa, which we induced with H₂O₂. This stressor determined increased levels of Hsp60 through a gene up-regulation mechanism involving NFkB-p65. Release of Hsp60 in the extracellular medium by the bronchial epithelial cells was also increased after H₂O₂ treatment in the absence of cell death.
conclusionsThis is the first report clearly pointing to participation of Hsps, particularly Hsp60, in COPD pathogenesis. Hsp60 induction by NFkB-p65 and its release by epithelial cells after oxidative stress can have a role in maintaining inflammation, e.g., by stimulating neutrophils activity. The data open new scenarios that might help in designing efficacious anti-inflammatory therapies centered on Hsp60 and applicable to COPD.
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