TAS2R activation promotes airway smooth muscle relaxation despite β(2)-adrenergic receptor tachyphylaxis.
Identifieur interne : 000347 ( PubMed/Checkpoint ); précédent : 000346; suivant : 000348TAS2R activation promotes airway smooth muscle relaxation despite β(2)-adrenergic receptor tachyphylaxis.
Auteurs : Steven S. An [États-Unis] ; Wayne C H. Wang ; Cynthia J. Koziol-White ; Kwangmi Ahn ; Danielle Y. Lee ; Richard C. Kurten ; Reynold A. Panettieri ; Stephen B. LiggettSource :
- American journal of physiology. Lung cellular and molecular physiology [ 1522-1504 ] ; 2012.
Descripteurs français
- KwdFr :
- Agonistes bêta-adrénergiques (pharmacologie), Animaux, Appareil respiratoire (), Appareil respiratoire (métabolisme), Chloroquine (pharmacologie), Chlorure de méthacholine (pharmacologie), Humains, Isoprénaline (pharmacologie), Muscles lisses (), Muscles lisses (physiologie), Phénomènes physiologiques respiratoires (), Relâchement musculaire (), Relâchement musculaire (physiologie), Récepteurs bêta-2 adrénergiques (métabolisme), Récepteurs couplés aux protéines G (agonistes), Récepteurs couplés aux protéines G (métabolisme), Salbutamol (pharmacologie), Souris, Tachyphylaxie (physiologie), Techniques in vitro.
- MESH :
- agonistes : Récepteurs couplés aux protéines G.
- métabolisme : Appareil respiratoire, Récepteurs bêta-2 adrénergiques, Récepteurs couplés aux protéines G.
- pharmacologie : Agonistes bêta-adrénergiques, Chloroquine, Chlorure de méthacholine, Isoprénaline, Salbutamol.
- physiologie : Muscles lisses, Relâchement musculaire, Tachyphylaxie.
- Animaux, Appareil respiratoire, Humains, Muscles lisses, Phénomènes physiologiques respiratoires, Relâchement musculaire, Souris, Techniques in vitro.
English descriptors
- KwdEn :
- Adrenergic beta-Agonists (pharmacology), Albuterol (pharmacology), Animals, Chloroquine (pharmacology), Humans, In Vitro Techniques, Isoproterenol (pharmacology), Methacholine Chloride (pharmacology), Mice, Muscle Relaxation (drug effects), Muscle Relaxation (physiology), Muscle, Smooth (drug effects), Muscle, Smooth (physiology), Receptors, Adrenergic, beta-2 (metabolism), Receptors, G-Protein-Coupled (agonists), Receptors, G-Protein-Coupled (metabolism), Respiratory Physiological Phenomena (drug effects), Respiratory System (drug effects), Respiratory System (metabolism), Tachyphylaxis (physiology).
- MESH :
- chemical , agonists : Receptors, G-Protein-Coupled.
- chemical , metabolism : Receptors, Adrenergic, beta-2, Receptors, G-Protein-Coupled.
- chemical , pharmacology : Adrenergic beta-Agonists, Albuterol, Chloroquine, Isoproterenol, Methacholine Chloride.
- drug effects : Muscle Relaxation, Muscle, Smooth, Respiratory Physiological Phenomena, Respiratory System.
- metabolism : Respiratory System.
- physiology : Muscle Relaxation, Muscle, Smooth, Tachyphylaxis.
- Animals, Humans, In Vitro Techniques, Mice.
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.
DOI: 10.1152/ajplung.00126.2012
PubMed: 22683571
Affiliations:
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Lung cellular and molecular physiology</title><idno type="eISSN">1522-1504</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenergic beta-Agonists (pharmacology)</term><term>Albuterol (pharmacology)</term><term>Animals</term><term>Chloroquine (pharmacology)</term><term>Humans</term><term>In Vitro Techniques</term><term>Isoproterenol (pharmacology)</term><term>Methacholine Chloride (pharmacology)</term><term>Mice</term><term>Muscle Relaxation (drug effects)</term><term>Muscle Relaxation (physiology)</term><term>Muscle, Smooth (drug effects)</term><term>Muscle, Smooth (physiology)</term><term>Receptors, Adrenergic, beta-2 (metabolism)</term><term>Receptors, G-Protein-Coupled (agonists)</term><term>Receptors, G-Protein-Coupled (metabolism)</term><term>Respiratory Physiological Phenomena (drug effects)</term><term>Respiratory System (drug effects)</term><term>Respiratory System (metabolism)</term><term>Tachyphylaxis (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Agonistes bêta-adrénergiques (pharmacologie)</term><term>Animaux</term><term>Appareil respiratoire ()</term><term>Appareil respiratoire (métabolisme)</term><term>Chloroquine (pharmacologie)</term><term>Chlorure de méthacholine (pharmacologie)</term><term>Humains</term><term>Isoprénaline (pharmacologie)</term><term>Muscles lisses ()</term><term>Muscles lisses (physiologie)</term><term>Phénomènes physiologiques respiratoires ()</term><term>Relâchement musculaire ()</term><term>Relâchement musculaire (physiologie)</term><term>Récepteurs bêta-2 adrénergiques (métabolisme)</term><term>Récepteurs couplés aux protéines G (agonistes)</term><term>Récepteurs couplés aux protéines G (métabolisme)</term><term>Salbutamol (pharmacologie)</term><term>Souris</term><term>Tachyphylaxie (physiologie)</term><term>Techniques in vitro</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="metabolism" xml:lang="en"><term>Receptors, Adrenergic, beta-2</term><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adrenergic beta-Agonists</term><term>Albuterol</term><term>Chloroquine</term><term>Isoproterenol</term><term>Methacholine Chloride</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>Muscle Relaxation</term><term>Muscle, Smooth</term><term>Respiratory Physiological Phenomena</term><term>Respiratory System</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Respiratory System</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Appareil respiratoire</term><term>Récepteurs bêta-2 adrénergiques</term><term>Récepteurs couplés aux protéines G</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agonistes bêta-adrénergiques</term><term>Chloroquine</term><term>Chlorure de méthacholine</term><term>Isoprénaline</term><term>Salbutamol</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Muscles lisses</term><term>Relâchement musculaire</term><term>Tachyphylaxie</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Muscle Relaxation</term><term>Muscle, Smooth</term><term>Tachyphylaxis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>In Vitro Techniques</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Appareil respiratoire</term><term>Humains</term><term>Muscles lisses</term><term>Phénomènes physiologiques respiratoires</term><term>Relâchement musculaire</term><term>Souris</term><term>Techniques in vitro</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22683571</PMID><DateCompleted><Year>2012</Year><Month>10</Month><Day>24</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1504</ISSN><JournalIssue CitedMedium="Internet"><Volume>303</Volume><Issue>4</Issue><PubDate><Year>2012</Year><Month>Aug</Month><Day>15</Day></PubDate></JournalIssue><Title>American journal of physiology. Lung cellular and molecular physiology</Title><ISOAbbreviation>Am. J. Physiol. Lung Cell Mol. Physiol.</ISOAbbreviation></Journal><ArticleTitle>TAS2R activation promotes airway smooth muscle relaxation despite β(2)-adrenergic receptor tachyphylaxis.</ArticleTitle><Pagination><MedlinePgn>L304-11</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajplung.00126.2012</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>An</LastName><ForeName>Steven S</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Program in Respiratory Biology and Lung Disease, Johns Hopkins University, Bloomberg School of Public Health, 615 N Wolfe St., Rm. E-7616, Baltimore, MD 21205, USA. san@jhsph.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Wayne C H</ForeName><Initials>WC</Initials></Author><Author ValidYN="Y"><LastName>Koziol-White</LastName><ForeName>Cynthia J</ForeName><Initials>CJ</Initials></Author><Author ValidYN="Y"><LastName>Ahn</LastName><ForeName>Kwangmi</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Danielle Y</ForeName><Initials>DY</Initials></Author><Author ValidYN="Y"><LastName>Kurten</LastName><ForeName>Richard C</ForeName><Initials>RC</Initials></Author><Author ValidYN="Y"><LastName>Panettieri</LastName><ForeName>Reynold A</ForeName><Initials>RA</Initials><Suffix>Jr</Suffix></Author><Author ValidYN="Y"><LastName>Liggett</LastName><ForeName>Stephen B</ForeName><Initials>SB</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL097796</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL104119</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL107361</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1RR029884</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL107361</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL045967</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>ES013508</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL071609</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL071609</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>06</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Lung Cell Mol Physiol</MedlineTA><NlmUniqueID>100901229</NlmUniqueID><ISSNLinking>1040-0605</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000318">Adrenergic beta-Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018343">Receptors, Adrenergic, beta-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D043562">Receptors, G-Protein-Coupled</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C406821">taste receptors, type 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0W5ETF9M2K</RegistryNumber><NameOfSubstance UI="D016210">Methacholine Chloride</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>L628TT009W</RegistryNumber><NameOfSubstance UI="D007545">Isoproterenol</NameOfSubstance></Chemical><Chemical><RegistryNumber>QF8SVZ843E</RegistryNumber><NameOfSubstance UI="D000420">Albuterol</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Am J Physiol Lung Cell Mol Physiol. 2012 Dec 1;303(11):L953-5</RefSource><PMID Version="1">23023969</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000318" MajorTopicYN="N">Adrenergic beta-Agonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000420" MajorTopicYN="N">Albuterol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007545" MajorTopicYN="N">Isoproterenol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016210" MajorTopicYN="N">Methacholine Chloride</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009126" MajorTopicYN="N">Muscle Relaxation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009130" MajorTopicYN="N">Muscle, Smooth</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018343" MajorTopicYN="N">Receptors, Adrenergic, beta-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D043562" MajorTopicYN="N">Receptors, G-Protein-Coupled</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012143" MajorTopicYN="Y">Respiratory Physiological Phenomena</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012137" MajorTopicYN="N">Respiratory System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013618" MajorTopicYN="N">Tachyphylaxis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>10</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22683571</ArticleId><ArticleId IdType="pii">ajplung.00126.2012</ArticleId><ArticleId IdType="doi">10.1152/ajplung.00126.2012</ArticleId><ArticleId IdType="pmc">PMC3423830</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Nature. 2002 Aug 8;418(6898):591</Citation><ArticleIdList><ArticleId 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