ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
TAS2R activation promotes airway smooth muscle relaxation despite β(2)-adrenergic receptor tachyphylaxis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 88 citations in OpenAlex.
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- TMEM16A Antagonism: Therapeutic Potential with Desensitization of β-Agonist Responsiveness in Asthma.American journal of respiratory cell and molecular biology · 2025Article
- A-Kinase-Anchoring Protein Subtypes Differentially Regulate GPCR Signaling and Function in Human Airway Smooth Muscle.American journal of respiratory cell and molecular biology · 2025Article
- Ectopic taste receptors in animal physiology: evolutionary conservation and functional diversification.Frontiers in cell and developmental biology · 2025Review
- Precision cut lung slices: an integrated ex vivo model for studying lung physiology, pharmacology, disease pathogenesis and drug discovery.Respiratory research · 2024Review
- Perspectives on precision cut lung slices-powerful tools for investigation of mechanisms and therapeutic targets in lung diseases.Frontiers in pharmacology · 2023Review
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- Epinephrine evokes shortening of human airway smooth muscle cells following βAmerican journal of physiology. Lung cellular and molecular physiology · 2022Article
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- Bitter Taste Receptors in the Airway Cells Functions.Handbook of experimental pharmacology · 2022Article
- Identification and characterization of an atypical Gαs-biased βProceedings of the National Academy of Sciences of the United States of America · 2021Article
- An update on extra-oral bitter taste receptors.Journal of translational medicine · 2021Review
- Genetic deletion of the Tas2r143/Tas2r135/Tas2r126 cluster reveals that TAS2Rs may not mediate bitter tastant-induced bronchodilation.Journal of cellular physiology · 2021Article
- Chloroquine and COVID-19: role as a bitter taste receptor agonist?New microbes and new infections · 2021Article
- Vanillin Activates Human Bitter Taste Receptors TAS2R14, TAS2R20, and TAS2R39.Frontiers in nutrition · 2021Article
- Can GPCRs Be Targeted to Control Inflammation in Asthma?Advances in experimental medicine and biology · 2021Article
- Identification and Characterization of Novel Bronchodilator Agonists Acting at Human Airway Smooth Muscle Cell TAS2R5.ACS pharmacology & translational science · 2020Article
- The odorant receptor OR2W3 on airway smooth muscle evokes bronchodilation via a cooperative chemosensory tradeoff between TMEM16A and CFTR.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Therapeutic potential and challenges of bitter taste receptors on lung cells.Current opinion in pharmacology · 2020Review
- Tissue traction microscopy to quantify muscle contraction within precision-cut lung slices.American journal of physiology. Lung cellular and molecular physiology · 2020Article
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8 authors at 6 institutions in 1 country.
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Abstract
Recently, bitter taste receptors (TAS2Rs) were found in the lung and act to relax airway smooth muscle (ASM) via intracellular Ca(2+) concentration signaling generated from restricted phospholipase C activation. As potential therapy, TAS2R agonists could be add-on treatment when patients fail to achieve adequate bronchodilation with chronic β-agonists. The β(2)-adrenergic receptor (β(2)AR) of ASM undergoes extensive functional desensitization. It remains unknown whether this desensitization affects TAS2R function, by cross talk at the receptors or distal common components in the relaxation machinery. We studied intracellular signaling and cell mechanics using isolated human ASM, mouse tracheal responses, and human bronchial responses to characterize TAS2R relaxation in the context of β(2)AR desensitization. In isolated human ASM, magnetic twisting cytometry revealed >90% loss of isoproterenol-promoted decrease in cell stiffness after 18-h exposure to albuterol. Under these same conditions of β(2)AR desensitization, the TAS2R agonist chloroquine relaxation response was unaffected. TAS2R-mediated stimulation of intracellular Ca(2+) concentration in human ASM was unaltered by albuterol pretreatment, in contrast to cAMP signaling, which was desensitized by >90%. In mouse trachea, β(2)AR desensitization by β-agonist amounted to 92 ± 6.0% (P < 0.001), while, under these same conditions, TAS2R desensitization was not significant (11 ± 3.5%). In human lung slices, chronic β-agonist exposure culminated in 64 ± 5.7% (P < 0.001) desensitization of β(2)AR-mediated dilation of carbachol-constricted airways that was reversed by chloroquine. We conclude that there is no evidence for physiologically relevant cross-desensitization of TAS2R-mediated ASM relaxation from chronic β-agonist treatment. These findings portend a favorable therapeutic profile for TAS2R agonists for the treatment of bronchospasm in asthma or chronic obstructive lung disease.
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