cAMP has distinct acute and chronic effects on aquaporin-5 in lung epithelial cells.
Identifieur interne : 001E08 ( Main/Exploration ); précédent : 001E07; suivant : 001E09cAMP has distinct acute and chronic effects on aquaporin-5 in lung epithelial cells.
Auteurs : Venkataramana Sidhaye [États-Unis] ; Jason D. Hoffert ; Landon S. KingSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 2005.
Descripteurs français
- KwdFr :
- AMP cyclique (métabolisme), Agonistes bêta-adrénergiques (pharmacologie), Animaux, Aquaporine-5, Aquaporines (métabolisme), Cellules épithéliales (), Cellules épithéliales (cytologie), Cellules épithéliales (métabolisme), Eau (métabolisme), Homéostasie (physiologie), Poumon (cytologie), Protéines membranaires (métabolisme), Souris, Terbutaline (pharmacologie), Trachée (cytologie).
- MESH :
- cytologie : Cellules épithéliales, Poumon, Trachée.
- métabolisme : AMP cyclique, Aquaporines, Cellules épithéliales, Eau, Protéines membranaires.
- pharmacologie : Agonistes bêta-adrénergiques, Terbutaline.
- physiologie : Homéostasie.
- Animaux, Aquaporine-5, Cellules épithéliales, Souris.
English descriptors
- KwdEn :
- Adrenergic beta-Agonists (pharmacology), Animals, Aquaporin 5, Aquaporins (metabolism), Cyclic AMP (metabolism), Epithelial Cells (cytology), Epithelial Cells (drug effects), Epithelial Cells (metabolism), Homeostasis (physiology), Lung (cytology), Membrane Proteins (metabolism), Mice, Terbutaline (pharmacology), Trachea (cytology), Water (metabolism).
- MESH :
- chemical , metabolism : Aquaporins, Cyclic AMP, Membrane Proteins, Water.
- chemical , pharmacology : Adrenergic beta-Agonists, Terbutaline.
- cytology : Epithelial Cells, Lung, Trachea.
- drug effects : Epithelial Cells.
- metabolism : Epithelial Cells.
- physiology : Homeostasis.
- Animals, Aquaporin 5, Mice.
Abstract
Aquaporin-5 (AQP5) is present on the apical membrane of epithelial cells in various secretory glands as well as on the apical membrane of the airway epithelium, airway submucosal glands, and type 1 pneumocytes, where it can participate in respiratory tract water homeostasis. We examined the effects of cAMP on AQP5 distribution and abundance. When AQP5-expressing mouse lung epithelial cells were treated with cAMP or the beta-adrenergic agonist terbutaline, a biphasic AQP5 response was observed. Short term (minutes) exposure to cAMP produced internalization of AQP5 off of the membrane and a decrease in protein abundance. Both of these responses were blocked by inhibition of protein kinase A and the decrease in abundance was blocked by chloroquine, indicating lysosome-mediated degradation. Sustained cAMP exposure (hours) produced an increase in membrane localization and increased abundance; these effects were also blocked by protein kinase A inhibition. The beta-adrenergic agonist terbutaline produced changes in AQP5 abundance in mouse trachea and lung, consistent with our findings in cultured epithelial cells. Purified AQP5 protein was phosphorylated by protein kinase A but not protein kinase C or casein kinase II, and aquaporin-5 was phosphorylated in cultured cells after long term (but not short term) exposure to cAMP. These studies indicate that cAMP and beta-adrenergic agonists produce distinct short and long term effects on AQP5 distribution and abundance that may contribute to regulation of lung water homeostasis.
DOI: 10.1074/jbc.M411038200
PubMed: 15536076
Affiliations:
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Le document en format XML
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<term>Aquaporins (metabolism)</term>
<term>Cyclic AMP (metabolism)</term>
<term>Epithelial Cells (cytology)</term>
<term>Epithelial Cells (drug effects)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Homeostasis (physiology)</term>
<term>Lung (cytology)</term>
<term>Membrane Proteins (metabolism)</term>
<term>Mice</term>
<term>Terbutaline (pharmacology)</term>
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<term>Aquaporines (métabolisme)</term>
<term>Cellules épithéliales ()</term>
<term>Cellules épithéliales (cytologie)</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Eau (métabolisme)</term>
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<term>Protéines membranaires</term>
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<front><div type="abstract" xml:lang="en">Aquaporin-5 (AQP5) is present on the apical membrane of epithelial cells in various secretory glands as well as on the apical membrane of the airway epithelium, airway submucosal glands, and type 1 pneumocytes, where it can participate in respiratory tract water homeostasis. We examined the effects of cAMP on AQP5 distribution and abundance. When AQP5-expressing mouse lung epithelial cells were treated with cAMP or the beta-adrenergic agonist terbutaline, a biphasic AQP5 response was observed. Short term (minutes) exposure to cAMP produced internalization of AQP5 off of the membrane and a decrease in protein abundance. Both of these responses were blocked by inhibition of protein kinase A and the decrease in abundance was blocked by chloroquine, indicating lysosome-mediated degradation. Sustained cAMP exposure (hours) produced an increase in membrane localization and increased abundance; these effects were also blocked by protein kinase A inhibition. The beta-adrenergic agonist terbutaline produced changes in AQP5 abundance in mouse trachea and lung, consistent with our findings in cultured epithelial cells. Purified AQP5 protein was phosphorylated by protein kinase A but not protein kinase C or casein kinase II, and aquaporin-5 was phosphorylated in cultured cells after long term (but not short term) exposure to cAMP. These studies indicate that cAMP and beta-adrenergic agonists produce distinct short and long term effects on AQP5 distribution and abundance that may contribute to regulation of lung water homeostasis.</div>
</front>
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