Impaired Relaxation of Airway Smooth Muscle in Mice Lacking the Actin-Binding Protein Gelsolin.
Identifieur interne : 000D14 ( Main/Exploration ); précédent : 000D13; suivant : 000D15Impaired Relaxation of Airway Smooth Muscle in Mice Lacking the Actin-Binding Protein Gelsolin.
Auteurs : Maya Mikami [États-Unis] ; Yi Zhang [États-Unis] ; Jennifer Danielsson [États-Unis] ; Tiarra Joell [États-Unis] ; Hwan Mee Yong [États-Unis] ; Elizabeth Townsend [États-Unis] ; Seema Khurana ; Steven S. An [États-Unis] ; Charles W. Emala [États-Unis]Source :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2017.
Descripteurs français
- KwdFr :
- Actines (métabolisme), Animaux, Chloroquine (pharmacologie), Gelsoline (métabolisme), Impédance électrique, Inositol phosphates (métabolisme), Muscles lisses (), Muscles lisses (physiologie), Myocytes du muscle lisse (), Myocytes du muscle lisse (métabolisme), Mâle, Phénomènes biomécaniques (), Poumon (), Poumon (physiologie), Relâchement musculaire (), Relâchement musculaire (physiologie), Récepteurs couplés aux protéines G (antagonistes et inhibiteurs), Récepteurs couplés aux protéines G (métabolisme), Souris de lignée C57BL, Souris knockout, Séparation cellulaire.
- MESH :
- antagonistes et inhibiteurs : Récepteurs couplés aux protéines G.
- métabolisme : Actines, Gelsoline, Inositol phosphates, Myocytes du muscle lisse, Récepteurs couplés aux protéines G.
- pharmacologie : Chloroquine.
- physiologie : Muscles lisses, Poumon, Relâchement musculaire.
- Animaux, Impédance électrique, Muscles lisses, Myocytes du muscle lisse, Mâle, Phénomènes biomécaniques, Poumon, Relâchement musculaire, Souris de lignée C57BL, Souris knockout, Séparation cellulaire.
English descriptors
- KwdEn :
- Actins (metabolism), Animals, Biomechanical Phenomena (drug effects), Cell Separation, Chloroquine (pharmacology), Electric Impedance, Gelsolin (metabolism), Inositol Phosphates (metabolism), Lung (drug effects), Lung (physiology), Male, Mice, Inbred C57BL, Mice, Knockout, Muscle Relaxation (drug effects), Muscle Relaxation (physiology), Muscle, Smooth (drug effects), Muscle, Smooth (physiology), Myocytes, Smooth Muscle (drug effects), Myocytes, Smooth Muscle (metabolism), Receptors, G-Protein-Coupled (antagonists & inhibitors), Receptors, G-Protein-Coupled (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Receptors, G-Protein-Coupled.
- chemical , metabolism : Actins, Gelsolin, Inositol Phosphates, Receptors, G-Protein-Coupled.
- drug effects : Biomechanical Phenomena, Lung, Muscle Relaxation, Muscle, Smooth, Myocytes, Smooth Muscle.
- metabolism : Myocytes, Smooth Muscle.
- chemical , pharmacology : Chloroquine.
- physiology : Lung, Muscle Relaxation, Muscle, Smooth.
- Animals, Cell Separation, Electric Impedance, Male, Mice, Inbred C57BL, Mice, Knockout.
Abstract
Diverse classes of ligands have recently been discovered that relax airway smooth muscle (ASM) despite a transient increase in intracellular calcium concentrations ([Ca2+]i). However, the cellular mechanisms are not well understood. Gelsolin is a calcium-activated actin-severing and -capping protein found in many cell types, including ASM cells. Gelsolin also binds to phosphatidylinositol 4,5-bisphosphate, making this substrate less available for phospholipase Cβ-mediated hydrolysis to inositol triphosphate and diacylglycerol. We hypothesized that gelsolin plays a critical role in ASM relaxation and mechanistically accounts for relaxation by ligands that transiently increase [Ca2+]i. Isolated tracheal rings from gelsolin knockout (KO) mice showed impaired relaxation to both a β-agonist and chloroquine, a bitter taste receptor agonist, which relaxes ASM, despite inducing transiently increased [Ca2+]i. A single inhalation of methacholine increased lung resistance to a similar extent in wild-type and gelsolin KO mice, but the subsequent spontaneous relaxation was less in gelsolin KO mice. In ASM cells derived from gelsolin KO mice, serotonin-induced Gq-coupled activation increased both [Ca2+]i and inositol triphosphate synthesis to a greater extent compared to cells from wild-type mice, possibly due to the absence of gelsolin binding to phosphatidylinositol 4,5-bisphosphate. Single-cell analysis showed higher filamentous:globular actin ratio at baseline and slower cytoskeletal remodeling dynamics in gelsolin KO cells. Gelsolin KO ASM cells also showed an attenuated decrease in cell stiffness to chloroquine and flufenamic acid. These findings suggest that gelsolin plays a critical role in ASM relaxation and that activation of gelsolin may contribute to relaxation induced by ligands that relax ASM despite a transient increase in [Ca2+]i.
DOI: 10.1165/rcmb.2016-0292OC
PubMed: 28118027
Affiliations:
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York</region></placeName><wicri:cityArea>1 Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York</wicri:cityArea></affiliation></author><author><name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name><affiliation wicri:level="2"><nlm:affiliation>1 Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>1 Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York</wicri:cityArea></affiliation></author><author><name sortKey="Danielsson, Jennifer" sort="Danielsson, Jennifer" uniqKey="Danielsson J" first="Jennifer" last="Danielsson">Jennifer Danielsson</name><affiliation wicri:level="2"><nlm:affiliation>1 Department of Anesthesiology, College of Physicians and Surgeons, 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Columbia University, New York</wicri:cityArea></affiliation></author><author><name sortKey="Khurana, Seema" sort="Khurana, Seema" uniqKey="Khurana S" first="Seema" last="Khurana">Seema Khurana</name><affiliation><nlm:affiliation>3 Department of Biology and Biochemistry, University of Houston, Baylor College of Medicine, Houston, Texas; and.</nlm:affiliation><wicri:noCountry code="subField">Texas; and</wicri:noCountry></affiliation></author><author><name sortKey="An, Steven S" sort="An, Steven S" uniqKey="An S" first="Steven S" last="An">Steven S. 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Emala</name><affiliation wicri:level="2"><nlm:affiliation>1 Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>1 Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York</wicri:cityArea></affiliation></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Actins (metabolism)</term><term>Animals</term><term>Biomechanical Phenomena (drug effects)</term><term>Cell Separation</term><term>Chloroquine (pharmacology)</term><term>Electric Impedance</term><term>Gelsolin (metabolism)</term><term>Inositol Phosphates (metabolism)</term><term>Lung (drug effects)</term><term>Lung (physiology)</term><term>Male</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Muscle Relaxation (drug effects)</term><term>Muscle Relaxation (physiology)</term><term>Muscle, Smooth (drug effects)</term><term>Muscle, Smooth (physiology)</term><term>Myocytes, Smooth Muscle (drug effects)</term><term>Myocytes, Smooth Muscle (metabolism)</term><term>Receptors, G-Protein-Coupled (antagonists & inhibitors)</term><term>Receptors, G-Protein-Coupled (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Actines (métabolisme)</term><term>Animaux</term><term>Chloroquine (pharmacologie)</term><term>Gelsoline (métabolisme)</term><term>Impédance électrique</term><term>Inositol phosphates (métabolisme)</term><term>Muscles lisses ()</term><term>Muscles lisses (physiologie)</term><term>Myocytes du muscle lisse ()</term><term>Myocytes du muscle lisse (métabolisme)</term><term>Mâle</term><term>Phénomènes biomécaniques ()</term><term>Poumon ()</term><term>Poumon (physiologie)</term><term>Relâchement musculaire ()</term><term>Relâchement musculaire (physiologie)</term><term>Récepteurs couplés aux protéines G (antagonistes et inhibiteurs)</term><term>Récepteurs couplés aux protéines G (métabolisme)</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Séparation cellulaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Actins</term><term>Gelsolin</term><term>Inositol Phosphates</term><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteurs couplés aux protéines G</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Biomechanical Phenomena</term><term>Lung</term><term>Muscle Relaxation</term><term>Muscle, Smooth</term><term>Myocytes, Smooth Muscle</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Myocytes, Smooth Muscle</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Actines</term><term>Gelsoline</term><term>Inositol phosphates</term><term>Myocytes du muscle lisse</term><term>Récepteurs couplés aux protéines G</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Muscles lisses</term><term>Poumon</term><term>Relâchement musculaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lung</term><term>Muscle Relaxation</term><term>Muscle, Smooth</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Separation</term><term>Electric Impedance</term><term>Male</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Impédance électrique</term><term>Muscles lisses</term><term>Myocytes du muscle lisse</term><term>Mâle</term><term>Phénomènes biomécaniques</term><term>Poumon</term><term>Relâchement musculaire</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Séparation cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Diverse classes of ligands have recently been discovered that relax airway smooth muscle (ASM) despite a transient increase in intracellular calcium concentrations ([Ca<sup>2+</sup>]<sub>i</sub>). However, the cellular mechanisms are not well understood. Gelsolin is a calcium-activated actin-severing and -capping protein found in many cell types, including ASM cells. Gelsolin also binds to phosphatidylinositol 4,5-bisphosphate, making this substrate less available for phospholipase Cβ-mediated hydrolysis to inositol triphosphate and diacylglycerol. We hypothesized that gelsolin plays a critical role in ASM relaxation and mechanistically accounts for relaxation by ligands that transiently increase [Ca<sup>2+</sup>]<sub>i</sub>. Isolated tracheal rings from gelsolin knockout (KO) mice showed impaired relaxation to both a β-agonist and chloroquine, a bitter taste receptor agonist, which relaxes ASM, despite inducing transiently increased [Ca<sup>2+</sup>]<sub>i</sub>. A single inhalation of methacholine increased lung resistance to a similar extent in wild-type and gelsolin KO mice, but the subsequent spontaneous relaxation was less in gelsolin KO mice. In ASM cells derived from gelsolin KO mice, serotonin-induced Gq-coupled activation increased both [Ca<sup>2+</sup>]<sub>i</sub> and inositol triphosphate synthesis to a greater extent compared to cells from wild-type mice, possibly due to the absence of gelsolin binding to phosphatidylinositol 4,5-bisphosphate. Single-cell analysis showed higher filamentous:globular actin ratio at baseline and slower cytoskeletal remodeling dynamics in gelsolin KO cells. Gelsolin KO ASM cells also showed an attenuated decrease in cell stiffness to chloroquine and flufenamic acid. These findings suggest that gelsolin plays a critical role in ASM relaxation and that activation of gelsolin may contribute to relaxation induced by ligands that relax ASM despite a transient increase in [Ca<sup>2+</sup>]<sub>i</sub>.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li><li>État de New York</li></region></list><tree><noCountry><name sortKey="Khurana, Seema" sort="Khurana, Seema" uniqKey="Khurana S" first="Seema" last="Khurana">Seema Khurana</name></noCountry><country name="États-Unis"><region name="État de New York"><name sortKey="Mikami, Maya" sort="Mikami, Maya" uniqKey="Mikami M" first="Maya" last="Mikami">Maya Mikami</name></region><name sortKey="An, Steven S" sort="An, Steven S" uniqKey="An S" first="Steven S" last="An">Steven S. An</name><name sortKey="Danielsson, Jennifer" sort="Danielsson, Jennifer" uniqKey="Danielsson J" first="Jennifer" last="Danielsson">Jennifer Danielsson</name><name sortKey="Emala, Charles W" sort="Emala, Charles W" uniqKey="Emala C" first="Charles W" last="Emala">Charles W. Emala</name><name sortKey="Joell, Tiarra" sort="Joell, Tiarra" uniqKey="Joell T" first="Tiarra" last="Joell">Tiarra Joell</name><name sortKey="Townsend, Elizabeth" sort="Townsend, Elizabeth" uniqKey="Townsend E" first="Elizabeth" last="Townsend">Elizabeth Townsend</name><name sortKey="Yong, Hwan Mee" sort="Yong, Hwan Mee" uniqKey="Yong H" first="Hwan Mee" last="Yong">Hwan Mee Yong</name><name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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