ArticleMolecular biology reports2014
The role of bronchial epithelial cell apoptosis in the pathogenesis of COPD.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Natural killer cells in the lung: novel insight and future challenge in the airway diseases.ERJ open research · 2025Review
- TET1 Alleviates Cigarette Smoke Induced Bronchial Epithelial Cell Apoptosis Through Upregulating Nrf2.International journal of chronic obstructive pulmonary disease · 2025Article
- The Relationship Between Hypothyroidism and Pneumonia and Possible Prevention and Treatment Measures.International journal of general medicine · 2025Article
- Modulating mitochondria with natural extract compounds: from bench to clinical therapeutic opportunities for COPD.Frontiers in pharmacology · 2025Review
- Therapeutic effects of melatonin on the lungs of rats exposed to passive smoking.Respiratory research · 2024Article
- Increased Lipocalin 2 detected by RNA sequencing regulates apoptosis and ferroptosis in COPD.BMC pulmonary medicine · 2024Article
- CTNNAL1 promotes the structural integrity of bronchial epithelial cells through the RhoA/ROCK1 pathway.Acta biochimica et biophysica Sinica · 2024Article
- Article
- CXCR4 enhances the inhibitory effects of bone mesenchymal stem cells on lung cell apoptosis in a rat model of smoking-induced COPD.Apoptosis : an international journal on programmed cell death · 2023Article
- Biological and Genetic Mechanisms of COPD, Its Diagnosis, Treatment, and Relationship with Lung Cancer.Biomedicines · 2023Review
- The effect of multiple outgrowths from bronchial tissue explants on progenitor/stem cell number in primary bronchial epithelial cell cultures from smokers and patients with COPD.Frontiers in medicine · 2023Article
- Effect of pirfenidone protecting against cigarette smoke extract induced apoptosis.Tobacco induced diseases · 2022Article
- Capsaicin suppresses ciliary function, while inducing permeability in bronchial epithelial cell cultures of COPD patients.Frontiers in pharmacology · 2022Article
- Impact of cathepsin D activity and C224T polymorphism (rs17571) on chronic obstructive pulmonary disease: correlations with oxidative and inflammatory markers.Clinical and experimental medicine · 2021Article
- The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD.Scientific reports · 2021Article
- The DNA methylation of FOXO3 and TP53 as a blood biomarker of late-onset asthma.Journal of translational medicine · 2020Article
- Alantolactone suppresses inflammation, apoptosis and oxidative stress in cigarette smoke-induced human bronchial epithelial cells through activation of Nrf2/HO-1 and inhibition of the NF-κB pathways.Respiratory research · 2020Article
- Xiaoqinglong Decoction Protects the Lungs of AECOPD Mice through the AMPK/mTOR Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Jianpiyifei II Granules Suppress Apoptosis of Bronchial Epithelial Cells in Chronic Obstructive Pulmonary DiseaseFrontiers in pharmacology · 2020Article
- PMEnvironmental science and pollution research international · 2019Article
Corrections and comments
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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
There is an increased airway inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD), and it has been suggested that there may also be problem in the apoptosis and renewal of cells. However, there are limited human airway cell studies, in particular those from larger airways such as bronchi. We cultured primary human bronchial epithelial cells (HBECs) from bronchial explants of smokers (n = 6) without COPD and smokers with COPD (n = 8). Apoptosis was studied by fluorescence activated cell sorting. qRT-PCR was used to assess mRNA expression for proteins involving apoptosis including p21(CIP1/WAF1), p53, caspase-8 and caspase-9. Although there was no difference in the rate of viable cells between cells from smokers and COPDs, the level of early apoptotic cells was significantly increased in COPD cells [mean ± standard error of mean (SEM) = 4.86 ± 3.2 %, p = 0.015] as compared to smokers (mean ± SEM = 2.71 ± 1.62 %). In contrast, the rate of late apoptotic cells was significantly decreased in COPD cells (mean ± SEM = 9.82 ± 5.71 %) comparing to smokers (mean ± SEM = 15.21 ± 5.08 %, p = 0.003). Although expression of mRNA for p21(CIP1/WAF1) and caspase-9 was similar in both groups, p53 and caspase-8 mRNA expression was significantly greater in COPD cells. These findings suggest that HBEC apoptosis is increased in COPD, and that this involves p53 and caspase-8 pathways.
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