ArticleScientific reports2018
A Small Molecule BH3-mimetic Suppresses Cigarette Smoke-Induced Mucous Expression in Airway Epithelial Cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- ACE-2 blockade and TMPRSS2 inhibition mitigate SARS-CoV-2 severity following cigarette smoke exposure in airway epithelial cellsMolecular therapy. Nucleic acids · 2025Article
- Comparative transcriptomics in human COPD reveals dysregulated genes uniquely expressed in ferrets.Respiratory research · 2022Article
- The Delivery of mRNA Vaccines for Therapeutics.Life (Basel, Switzerland) · 2022Review
- Differential gene expression of 3D primary human airway cultures exposed to cigarette smoke and electronic nicotine delivery system (ENDS) preparations.BMC medical genomics · 2022Article
- Increased Expression ofFrontiers in immunology · 2022Article
- Autophagy Induced by BCL2-Related ceRNA Network Participates in the Occurrence of COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- HIV-1 Productively Infects and Integrates in Bronchial Epithelial Cells.Frontiers in cellular and infection microbiology · 2020Article
- Acetylcholinesterase Inhibitor Pyridostigmine Bromide Attenuates Gut Pathology and Bacterial Dysbiosis in a Murine Model of Ulcerative Colitis.Digestive diseases and sciences · 2020Article
- Escalating Mucus Inhibition to the Top of Our Priorities.American journal of respiratory cell and molecular biology · 2019Article
- Dual Role For A MEK Inhibitor As A Modulator Of Inflammation And Host Defense Mechanisms With Potential Therapeutic Application In COPD.International journal of chronic obstructive pulmonary disease · 2019Article
- Etanercept Protected Against Cigarette Smoke Extract-Induced Inflammation and Apoptosis of Human Pulmonary Artery Endothelial Cells via Regulating TNFR1.International journal of chronic obstructive pulmonary diseaseArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cigarette smoke (CS) exposure is one of the primary risk factors associated with the chronic mucous hypersecretion (CMH). The antiapoptotic protein, Bcl-2 sustains hyperplastic mucous cells, and the airway epithelium of ex-smokers with CMH as well as mice exposed to chronic CS showed increased Bcl-2 expression. Therefore, we investigated whether Bcl-2 plays a role in CS-induced mucous expression. Primary airway epithelial cells (AECs) of murine and human origin were treated with CS extract (CSE), and there was a concentration- and time-dependent increase in secretory mucin (MUC5AC), mucous regulator (SPDEF) and Bcl-2 expression. Using differentiated human AECs cultured on air-liquid interface, EGFR and ERK1/2 pathways were interrogated. Bcl-2 activity was blocked using a small molecule BH3 mimetic ABT-263 that disrupts the Bcl-2 interaction with pro-apoptotic proteins. The ABT-263 treatment resulted in the downregulation of CSE-induced mucus expression and disrupted the EGFR-signaling while inducing the apoptosis and the pro-apoptotic protein, Bik expression. This strategy significantly suppressed the mainstream CS-induced mucous phenotype in a 3-D human airway epithelium model. Therefore, the present study suggests that CS induces Bcl-2 expression to help promote mucous cell survival; and small molecule BH3 mimetics targeting Bcl-2 could be useful in suppressing the CS-induced mucous response.
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