ArticleInternational journal of chronic obstructive pulmonary disease2020
The Protective Effect of HBO1 on Cigarette Smoke Extract-Induced Apoptosis in Airway Epithelial Cells.
Article in International journal of chronic obstructive pulmonary disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 35 citations in OpenAlex.
- Bu-Fei Yi-Shen Formula Alleviates Oxidative Stress and Improves Airway Epithelial Barrier Dysfunction in COPD.International journal of chronic obstructive pulmonary disease · 2026Article
- Review
- YAP/TAZ-mediated nuclear membrane rupture in promoting senescence of skeletal muscle associated with COPD.Respiratory research · 2025Article
- H3K14: A histone site closely related to diseases.Journal of Cancer · 2025Review
- Multifunctional acyltransferase HBO1: a key regulatory factor for cellular functions.Cellular & molecular biology letters · 2024Review
- Cigarette smoke extract induces ferroptosis in human retinal pigment epithelial cells.Heliyon · 2024Article
- Review
- Astaxanthin attenuates cigarette smoke-induced small airway remodeling via the AKT1 signaling pathway.Respiratory research · 2024Article
- TET2 stabilized by deubiquitinase USP21 ameliorates cigarette smoke-induced apoptosis in airway epithelial cells.iScience · 2024Article
- PU.1 alleviates the inhibitory effects of cigarette smoke on endothelial progenitor cell function and lung-homing through Wnt/β-catenin and CXCL12/CXCR4 pathways.Tobacco induced diseases · 2024Article
- CAPN5 attenuates cigarette smoke extract-induced apoptosis and inflammation in BEAS-2B cells.Tobacco induced diseases · 2024Article
- Cigarette smoke aggravates asthma via altering airways inflammation phenotypes and remodelling.The clinical respiratory journal · 2023Article
- The circular RNANeural regeneration research · 2023Article
- CSE reduces OTUD4 triggering lung epithelial cell apoptosis via PAI-1 degradation.Cell death & disease · 2023Article
- Glycyl-l-histidyl-l-lysine-CuJournal of cachexia, sarcopenia and muscle · 2023Article
- MFG-E8 stabilized by deubiquitinase USP14 suppresses cigarette smoke-induced ferroptosis in bronchial epithelial cells.Cell death & disease · 2023Article
- Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD.Frontiers in immunology · 2023Review
- Long noncoding RNA HOTAIR facilitates pulmonary vascular endothelial cell apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD.Respiratory research · 2022Article
- Effect of pirfenidone protecting against cigarette smoke extract induced apoptosis.Tobacco induced diseases · 2022Article
- Decreased expression of endothelial cell specific molecule-1 in lung tissue in emphysematous mice and stable COPD patients.Iranian journal of basic medical sciences · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Epigenetic modification is one of most important mechanisms underlying the pathogenesis of chronic obstructive pulmonary disease (COPD). The purpose of this study was to determine whether histone acetyltransferase binding to ORC1 (HBO1) can protect against cigarette smoke (CS)-induced cell apoptosis and sustain normal histone acetylation in COPD. Methods: Human lung tissue samples were obtained from patients who underwent lung resection. The emphysema mouse model and HBO1 overexpressing mice were each established by intraperitoneal injection with cigarette smoke extract (CSE) or intratracheal lentiviral vectors instillation. TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assays were used to assess apoptotic ratio in mice. The apoptosis of human bronchial epithelial cells (HBECs) was assayed by flow cytometry. HBO1, B-cell lymphoma-2 (BCL-2), and H3K14ac protein expression were detected by Western blotting. HBO1 mRNA expression was measured by quantitative real-time polymerase chain reaction. Results: Protein expression of HBO1 was decreased significantly in lung tissue from COPD patients and CSE-treated emphysema mouse models. Overexpression of HBO1 attenuated CSE-induced emphysematous changes, as well as apoptosis in the lungs of COPD mice. In vitro, the HBO1 protein degraded in a time- and dose-dependent course with CSE treatment. With flow cytometry, we proved that HBO1 could reverse the apoptosis of HBECs induced by CSE. Furthermore, HBO1 overexpression promoted the expression of anti-apoptotic BCL-2 protein and enhanced H3K14 acetylation in airway epithelial cells. Conclusion: These findings demonstrate that the key histone modulator HBO1 plays a protective role in COPD pathogenesis that may shed light on potential therapeutic targets to inhibit the progress of COPD.
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