ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- Unraveling molecular mechanisms of cigarette smoke bitterness via chemical profiling and bitter taste receptor activation analysis.Scientific reports · 2025Article
- A deadly taste: linking bitter taste receptors and apoptosis.Apoptosis : an international journal on programmed cell death · 2025Review
- Characterization of Bitter Taste Receptor-Dependent Autophagy in Oral Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Article
- Exploring TAS2R46 biomechanics through molecular dynamics and network analysis.Frontiers in molecular biosciences · 2024Article
- Mitochondrial dynamics modulate the allergic inflammation in a murine model of allergic rhinitis.Immunity, inflammation and disease · 2023Article
- Article
- Tas2R activation relaxes airway smooth muscle by release of GαProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Impact of sweet, umami, and bitter taste receptor (TAS1R and TAS2R) genomic and expression alterations in solid tumors on survival.Scientific reports · 2022Article
- T2R bitter taste receptors regulate apoptosis and may be associated with survival in head and neck squamous cell carcinoma.Molecular oncology · 2022Article
- Bitter Taste Receptors in the Airway Cells Functions.Handbook of experimental pharmacology · 2022Article
- Diacylglycerol Kinase Inhibition Reduces Airway Contraction by Negative Feedback Regulation of Gq-Signaling.American journal of respiratory cell and molecular biology · 2021Article
- An update on extra-oral bitter taste receptors.Journal of translational medicine · 2021Review
- Chloroquine: Autophagy inhibitor, antimalarial, bitter taste receptor agonist in fight against COVID-19, a reality check?European journal of pharmacology · 2021Review
- Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come.Journal of asthma and allergy · 2021Review
- Mitochondrial dysfunction in lung ageing and disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Extreme Phenotype Approach Suggests Taste Transduction Pathway for Carotid Plaque in a Multi-Ethnic Cohort.Stroke · 2020Article
- Cytokine-induced molecular responses in airway smooth muscle cells inform genome-wide association studies of asthma.Genome medicine · 2020Article
- Therapeutic potential and challenges of bitter taste receptors on lung cells.Current opinion in pharmacology · 2020Review
- Chemosensory bitter taste receptors T2R4 and T2R14 activation attenuates proliferation and migration of breast cancer cells.Molecular and cellular biochemistry · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway remodeling, including increased airway smooth muscle (ASM) mass, is a hallmark feature of asthma and COPD. We previously identified the expression of bitter taste receptors (TAS2Rs) on human ASM cells and demonstrated that known TAS2R agonists could promote ASM relaxation and bronchodilation and inhibit mitogen-induced ASM growth. In this study, we explored cellular mechanisms mediating the antimitogenic effect of TAS2R agonists on human ASM cells. Pretreatment of ASM cells with TAS2R agonists chloroquine and quinine resulted in inhibition of cell survival, which was largely reversed by bafilomycin A1, an autophagy inhibitor. Transmission electron microscope studies demonstrated the presence of double-membrane autophagosomes and deformed mitochondria. In ASM cells, TAS2R agonists decreased mitochondrial membrane potential and increased mitochondrial ROS and mitochondrial fragmentation. Inhibiting dynamin-like protein 1 (DLP1) reversed TAS2R agonist-induced mitochondrial membrane potential change and attenuated mitochondrial fragmentation and cell death. Furthermore, the expression of mitochondrial protein BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (Bnip3) and mitochondrial localization of DLP1 were significantly upregulated by TAS2R agonists. More importantly, inhibiting Bnip3 mitochondrial localization by dominant-negative Bnip3 significantly attenuated cell death induced by TAS2R agonist. Collectively the TAS2R agonists chloroquine and quinine modulate mitochondrial structure and function, resulting in ASM cell death. Furthermore, Bnip3 plays a central role in TAS2R agonist-induced ASM functional changes via a mitochondrial pathway. These findings further establish the cellular mechanisms of antimitogenic effects of TAS2R agonists and identify a novel class of receptors and pathways that can be targeted to mitigate airway remodeling as well as bronchoconstriction in obstructive airway diseases.
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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.