Bitter taste receptor function in asthmatic and nonasthmatic human airway smooth muscle cells.
Identifieur interne : 001034 ( Main/Exploration ); précédent : 001033; suivant : 001035Bitter taste receptor function in asthmatic and nonasthmatic human airway smooth muscle cells.
Auteurs : Kathryn S. Robinett [États-Unis] ; Cynthia J. Koziol-White ; Arda Akoluk ; Steven S. An ; Reynold A. Panettieri ; Stephen B. LiggettSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2014.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Agonistes bêta-adrénergiques (pharmacologie), Appareil respiratoire (), Appareil respiratoire (métabolisme), Appareil respiratoire (physiopathologie), Asthme (métabolisme), Asthme (physiopathologie), Bronchoconstriction, Bronchodilatateurs (pharmacologie), Cellules cultivées, Cytosquelette (métabolisme), Goût, Humains, Interleukine-13 (métabolisme), Myocytes du muscle lisse (), Myocytes du muscle lisse (métabolisme), Médiateurs de l'inflammation (métabolisme), Récepteurs couplés aux protéines G (agonistes), Récepteurs couplés aux protéines G (génétique), Récepteurs couplés aux protéines G (métabolisme), Régulation de l'expression des gènes, Signalisation du calcium, Études cas-témoins.
- MESH :
- agonistes : Récepteurs couplés aux protéines G.
- génétique : Récepteurs couplés aux protéines G.
- métabolisme : ARN messager, Appareil respiratoire, Asthme, Cytosquelette, Interleukine-13, Myocytes du muscle lisse, Médiateurs de l'inflammation, Récepteurs couplés aux protéines G.
- pharmacologie : Agonistes bêta-adrénergiques, Bronchodilatateurs.
- physiopathologie : Appareil respiratoire, Asthme.
- Appareil respiratoire, Bronchoconstriction, Cellules cultivées, Goût, Humains, Myocytes du muscle lisse, Régulation de l'expression des gènes, Signalisation du calcium, Études cas-témoins.
English descriptors
- KwdEn :
- Adrenergic beta-Agonists (pharmacology), Asthma (metabolism), Asthma (physiopathology), Bronchoconstriction, Bronchodilator Agents (pharmacology), Calcium Signaling, Case-Control Studies, Cells, Cultured, Cytoskeleton (metabolism), Gene Expression Regulation, Humans, Inflammation Mediators (metabolism), Interleukin-13 (metabolism), Myocytes, Smooth Muscle (drug effects), Myocytes, Smooth Muscle (metabolism), RNA, Messenger (metabolism), Receptors, G-Protein-Coupled (agonists), Receptors, G-Protein-Coupled (genetics), Receptors, G-Protein-Coupled (metabolism), Respiratory System (drug effects), Respiratory System (metabolism), Respiratory System (physiopathology), Taste.
- MESH :
- chemical , agonists : Receptors, G-Protein-Coupled.
- chemical , genetics : Receptors, G-Protein-Coupled.
- chemical , metabolism : Inflammation Mediators, Interleukin-13, RNA, Messenger, Receptors, G-Protein-Coupled.
- chemical , pharmacology : Adrenergic beta-Agonists, Bronchodilator Agents.
- drug effects : Myocytes, Smooth Muscle, Respiratory System.
- metabolism : Asthma, Cytoskeleton, Myocytes, Smooth Muscle, Respiratory System.
- physiopathology : Asthma, Respiratory System.
- Bronchoconstriction, Calcium Signaling, Case-Control Studies, Cells, Cultured, Gene Expression Regulation, Humans, Taste.
Abstract
Bitter taste receptors (TAS2Rs) have recently been found to be expressed on human airway smooth muscle (HASM), and their activation results in marked relaxation. These agents have been proposed as a new class of bronchodilators in the treatment of obstructive lung diseases because they act via a different mechanism than β-agonists. The TAS2R signal transduction pathway in HASM has multiple elements that are potentially subject to regulation by inflammatory, genetic, and epigenetic mechanisms associated with asthma. To address this, expression, signaling, and physiologic functions of the three major TAS2Rs (subtypes 10, 14, and 31) on HASM were studied. Transcript expression of these TAS2Rs was not decreased in HASM cells derived from donors with asthma compared with those without asthma (n = 6 from each group). In addition, intracellular calcium ([Ca(2+)]i) signaling using TAS2R subtype-specific agonists (diphenhydramine, chloroquine, saccharin, and flufenamic acid) was not impaired in the cells derived from donors with asthma, nor was the response to quinine, which activates all three subtypes. HASM cell mechanics measured by magnetic twisting cytometry revealed equivalent TAS2R-mediated relaxation of methacholine-treated cells between the two groups. Human precision-cut lung slices treated with IL-13 caused a decrease in β-agonist (formoterol)-mediated relaxation of carbachol-contracted airways compared with control slices. In contrast, TAS2R-mediated relaxation was unaffected by IL-13. We conclude that TAS2R expression or function is unaffected in HASM cells derived from patients with asthma or the IL-13 inflammatory environment.
DOI: 10.1165/rcmb.2013-0439RC
PubMed: 24219573
Affiliations:
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Le document en format XML
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Koziol-White</name></author><author><name sortKey="Akoluk, Arda" sort="Akoluk, Arda" uniqKey="Akoluk A" first="Arda" last="Akoluk">Arda Akoluk</name></author><author><name sortKey="An, Steven S" sort="An, Steven S" uniqKey="An S" first="Steven S" last="An">Steven S. An</name></author><author><name sortKey="Panettieri, Reynold A" sort="Panettieri, Reynold A" uniqKey="Panettieri R" first="Reynold A" last="Panettieri">Reynold A. Panettieri</name></author><author><name sortKey="Liggett, Stephen B" sort="Liggett, Stephen B" uniqKey="Liggett S" first="Stephen B" last="Liggett">Stephen B. 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Robinett</name><affiliation wicri:level="2"><nlm:affiliation>1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Maryland School of Medicine, Baltimore, Maryland.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Koziol White, Cynthia J" sort="Koziol White, Cynthia J" uniqKey="Koziol White C" first="Cynthia J" last="Koziol-White">Cynthia J. Koziol-White</name></author><author><name sortKey="Akoluk, Arda" sort="Akoluk, Arda" uniqKey="Akoluk A" first="Arda" last="Akoluk">Arda Akoluk</name></author><author><name sortKey="An, Steven S" sort="An, Steven S" uniqKey="An S" first="Steven S" last="An">Steven S. An</name></author><author><name sortKey="Panettieri, Reynold A" sort="Panettieri, Reynold A" uniqKey="Panettieri R" first="Reynold A" last="Panettieri">Reynold A. Panettieri</name></author><author><name sortKey="Liggett, Stephen B" sort="Liggett, Stephen B" uniqKey="Liggett S" first="Stephen B" last="Liggett">Stephen B. Liggett</name></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenergic beta-Agonists (pharmacology)</term><term>Asthma (metabolism)</term><term>Asthma (physiopathology)</term><term>Bronchoconstriction</term><term>Bronchodilator Agents (pharmacology)</term><term>Calcium Signaling</term><term>Case-Control Studies</term><term>Cells, Cultured</term><term>Cytoskeleton (metabolism)</term><term>Gene Expression Regulation</term><term>Humans</term><term>Inflammation Mediators (metabolism)</term><term>Interleukin-13 (metabolism)</term><term>Myocytes, Smooth Muscle (drug effects)</term><term>Myocytes, Smooth Muscle (metabolism)</term><term>RNA, Messenger (metabolism)</term><term>Receptors, G-Protein-Coupled (agonists)</term><term>Receptors, G-Protein-Coupled (genetics)</term><term>Receptors, G-Protein-Coupled (metabolism)</term><term>Respiratory System (drug effects)</term><term>Respiratory System (metabolism)</term><term>Respiratory System (physiopathology)</term><term>Taste</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Agonistes bêta-adrénergiques (pharmacologie)</term><term>Appareil respiratoire ()</term><term>Appareil respiratoire (métabolisme)</term><term>Appareil respiratoire (physiopathologie)</term><term>Asthme (métabolisme)</term><term>Asthme (physiopathologie)</term><term>Bronchoconstriction</term><term>Bronchodilatateurs (pharmacologie)</term><term>Cellules cultivées</term><term>Cytosquelette (métabolisme)</term><term>Goût</term><term>Humains</term><term>Interleukine-13 (métabolisme)</term><term>Myocytes du muscle lisse ()</term><term>Myocytes du muscle lisse (métabolisme)</term><term>Médiateurs de l'inflammation (métabolisme)</term><term>Récepteurs couplés aux protéines G (agonistes)</term><term>Récepteurs couplés aux protéines G (génétique)</term><term>Récepteurs couplés aux protéines G (métabolisme)</term><term>Régulation de l'expression des gènes</term><term>Signalisation du calcium</term><term>Études cas-témoins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Inflammation Mediators</term><term>Interleukin-13</term><term>RNA, Messenger</term><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adrenergic beta-Agonists</term><term>Bronchodilator Agents</term></keywords><keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Récepteurs couplés aux protéines G</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Myocytes, Smooth Muscle</term><term>Respiratory System</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteurs couplés aux protéines G</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Asthma</term><term>Cytoskeleton</term><term>Myocytes, Smooth Muscle</term><term>Respiratory System</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Appareil respiratoire</term><term>Asthme</term><term>Cytosquelette</term><term>Interleukine-13</term><term>Myocytes du muscle lisse</term><term>Médiateurs de l'inflammation</term><term>Récepteurs couplés aux protéines G</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agonistes bêta-adrénergiques</term><term>Bronchodilatateurs</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Appareil respiratoire</term><term>Asthme</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Asthma</term><term>Respiratory System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Bronchoconstriction</term><term>Calcium Signaling</term><term>Case-Control Studies</term><term>Cells, Cultured</term><term>Gene Expression Regulation</term><term>Humans</term><term>Taste</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Appareil respiratoire</term><term>Bronchoconstriction</term><term>Cellules cultivées</term><term>Goût</term><term>Humains</term><term>Myocytes du muscle lisse</term><term>Régulation de l'expression des gènes</term><term>Signalisation du calcium</term><term>Études cas-témoins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bitter taste receptors (TAS2Rs) have recently been found to be expressed on human airway smooth muscle (HASM), and their activation results in marked relaxation. These agents have been proposed as a new class of bronchodilators in the treatment of obstructive lung diseases because they act via a different mechanism than β-agonists. The TAS2R signal transduction pathway in HASM has multiple elements that are potentially subject to regulation by inflammatory, genetic, and epigenetic mechanisms associated with asthma. To address this, expression, signaling, and physiologic functions of the three major TAS2Rs (subtypes 10, 14, and 31) on HASM were studied. Transcript expression of these TAS2Rs was not decreased in HASM cells derived from donors with asthma compared with those without asthma (n = 6 from each group). In addition, intracellular calcium ([Ca(2+)]i) signaling using TAS2R subtype-specific agonists (diphenhydramine, chloroquine, saccharin, and flufenamic acid) was not impaired in the cells derived from donors with asthma, nor was the response to quinine, which activates all three subtypes. HASM cell mechanics measured by magnetic twisting cytometry revealed equivalent TAS2R-mediated relaxation of methacholine-treated cells between the two groups. Human precision-cut lung slices treated with IL-13 caused a decrease in β-agonist (formoterol)-mediated relaxation of carbachol-contracted airways compared with control slices. In contrast, TAS2R-mediated relaxation was unaffected by IL-13. We conclude that TAS2R expression or function is unaffected in HASM cells derived from patients with asthma or the IL-13 inflammatory environment. </div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Akoluk, Arda" sort="Akoluk, Arda" uniqKey="Akoluk A" first="Arda" last="Akoluk">Arda Akoluk</name><name sortKey="An, Steven S" sort="An, Steven S" uniqKey="An S" first="Steven S" last="An">Steven S. An</name><name sortKey="Koziol White, Cynthia J" sort="Koziol White, Cynthia J" uniqKey="Koziol White C" first="Cynthia J" last="Koziol-White">Cynthia J. Koziol-White</name><name sortKey="Liggett, Stephen B" sort="Liggett, Stephen B" uniqKey="Liggett S" first="Stephen B" last="Liggett">Stephen B. Liggett</name><name sortKey="Panettieri, Reynold A" sort="Panettieri, Reynold A" uniqKey="Panettieri R" first="Reynold A" last="Panettieri">Reynold A. Panettieri</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Robinett, Kathryn S" sort="Robinett, Kathryn S" uniqKey="Robinett K" first="Kathryn S" last="Robinett">Kathryn S. Robinett</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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