ArticleAmerican journal of respiratory and critical care medicine2011
Cigarette smoke suppresses Bik to cause epithelial cell hyperplasia and mucous cell metaplasia.
Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis.The European respiratory journal · 2024Pooled it
- Cigarette smoke induces MUC5AC protein expression through the activation of Sp1.The Journal of biological chemistry · 2012Trial
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Persistence of emphysema following cessation of cigarette smoke exposure requires a susceptibility factor.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Reduced Bik expression drives low-grade airway inflammation and increased risk for COPD in females.The Journal of clinical investigation · 2024Article
- Bik promotes proteasomal degradation to control low-grade inflammation.The Journal of clinical investigation · 2023Article
- Nutriepigenomics in Environmental-Associated Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- Development of an Integrated Platform to Assess the Physicochemical and Toxicological Properties of Wood Combustion Particulate Matter.Chemical research in toxicology · 2022Article
- Cigarette smoke extract-mediated FABP4 upregulation suppresses viability and induces apoptosis, inflammation and oxidative stress of bronchial epithelial cells by activating p38 MAPK/MK2 signaling pathway.Journal of inflammation (London, England) · 2022Article
- Casein kinase II activates Bik to induce death of hyperplastic mucous cells in a cell cycle-dependent manner.Journal of cellular physiology · 2022Article
- Autophagy Induced by BCL2-Related ceRNA Network Participates in the Occurrence of COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- Reactive Oxygen Species and Antioxidative Defense in Chronic Obstructive Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Short-term whole body cigarette smoke exposure induces regional differences in cellular response in the mouse larynx.Toxicology reports · 2021Article
- Identification of novel epigenetic abnormalities as sputum biomarkers for lung cancer risk among smokers and COPD patients.Lung cancer (Amsterdam, Netherlands) · 2020Article
- Dissecting the cellular specificity of smoking effects and reconstructing lineages in the human airway epithelium.Nature communications · 2020Article
- Jumping on the Single-Cell RNA-Sequencing Bandwagon: Take Care Not to Put the Cart before the Horse.American journal of respiratory cell and molecular biology · 2020Article
- COVID-19, COPD, and AECOPD: Immunological, Epidemiological, and Clinical Aspects.Frontiers in medicine · 2020Review
- A Small Molecule BH3-mimetic Suppresses Cigarette Smoke-Induced Mucous Expression in Airway Epithelial Cells.Scientific reports · 2018Article
- IL-13 in LPS-Induced Inflammation Causes Bcl-2 Expression to Sustain Hyperplastic Mucous cells.Scientific reports · 2018Article
- Does the BCL-2 family member BIK control lung carcinogenesis?Molecular & cellular oncology · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleAberrant regulation of airway epithelial cell numbers in airways leads to increased mucous secretions in chronic lung diseases such as chronic bronchitis. Because the Bcl-2 family of proteins is crucial for airway epithelial homeostasis, identifying the players that reduce cigarette smoke (CS)-induced mucous cell metaplasia can help to develop effective therapies.
objectivesTo identify the Bcl-2 family of proteins that play a role in reducing CS-induced mucous cell metaplasia.
methodsWe screened for dysregulated expression of the Bcl-2 family members. MEASUREMENTS AND MAIN
resultsWe identified Bik to be significantly reduced in bronchial brushings of patients with chronic epithelial cell hyperplasia compared with nondiseased control subjects. Reduced Bik but increased MUC5AC mRNA levels were also detected when normal human airway epithelial cells (HAECs) were exposed to CS or when autopsy tissues from former smokers with and without chronic bronchitis were compared. Similarly, exposure of C57Bl/6 mice to CS resulted in increased numbers of epithelial and mucous cells per millimeter of basal lamina, along with reduced Bik but increased Muc5ac expression, and this change was sustained even when mice were allowed to recover in filtered air for 8 weeks. Restoring Bik expression significantly suppressed CS-induced mucous cell metaplasia in differentiated primary HAEC cultures and in airways of mice in vivo. Bik blocked nuclear translocation of phospho-ERK1/2 to induce apoptosis of HAECs. The conserved Leu61 within Bik and ERK1/2 activation were essential to induce cell death in hyperplastic mucous cells.
conclusionsThese studies show that CS suppresses Bik expression to block airway epithelia cell death and thereby increases epithelial cell hyperplasia in chronic bronchitis.
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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.