Transient receptor potential vanilloid 1 receptors mediate acid‐induced mucin secretion via Ca2+ influx in human airway epithelial cells
Identifieur interne : 002300 ( Main/Exploration ); précédent : 002299; suivant : 002301Transient receptor potential vanilloid 1 receptors mediate acid‐induced mucin secretion via Ca2+ influx in human airway epithelial cells
Auteurs : Hongmei Yu [République populaire de Chine] ; Qi Li [République populaire de Chine] ; Xiangdong Zhou [République populaire de Chine, Niger] ; Victor P. Kolosov [Russie] ; Juliy M. Perelman [Russie]Source :
- Journal of Biochemical and Molecular Toxicology [ 1095-6670 ] ; 2012-05.
English descriptors
- Teeft :
- Agonist, Airway, Asthma, Biochem, Breath condensate, Capsaicin, Capsazepine, Cell supernatants, Citric, Citric acid, Condensate, Control group, Dependently, Epithelial, Epithelial cells, Experimental record, Granule, Independent experiments, Muc5ac, Muc5ac protein, Muc5ac protein secretion, Muc5ac secretion, Mucin, Mucin granules, Mucin secretion, Mucociliary clearance, Mucus, Mucus exocytosis, Physiol, Present study, Receptor, Respir, Respir cell, Respir crit care, Secretion, Statistical results, Supernatant, Toxicology, Transient receptor, Trpv1, Trpv1 agonist capsaicin, Trpv1 antagonist capsazepine, Trpv1 channel opening, Trpv1 currents, Uorescence, Uorescence intensities, Vanilloid.
Abstract
Mucin hypersecretion is a key pathological feature of inflammatory respiratory diseases. Previous studies have reported that acids (gastroesophageal reflux or environmental exposure) induce many respiratory symptoms and are implicated in the pathophysiology of obstructive airway diseases. To understand these mechanisms, we measured acid‐induced mucin secretion in human bronchial epithelial cells. In the present study, acid induced inward currents of transient receptor potential vanilloid (TRPV)1 and mucin 5AC (MUC5AC) secretion dose dependently, which were inhibited by TRPV1 antagonist capsazepine in a concentration‐dependent manner. TRPV1 agonist capsaicin mediated a concentration‐dependent increase in TRPV1 inward currents and MUC5AC secretion. Furthermore, capsaicin enhanced acid‐induced TRPV1 inward currents and MUC5AC secretion. Acid‐induced Ca2+ influx was prevented by capsazepine dose dependently and enhanced by capsaicin. Pretreatment only with capsaicin also increased the Ca2+ concentration in a concentration‐dependent manner. These data suggest that pharmacological inhibition of calcium‐permeable TRPV1 receptors could be used to prevent acid‐induced mucin secretion, thereby providing a potential mechanism to reduce their toxicity. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:179–186, 2012; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.20413
Url:
DOI: 10.1002/jbt.20413
Affiliations:
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Previous studies have reported that acids (gastroesophageal reflux or environmental exposure) induce many respiratory symptoms and are implicated in the pathophysiology of obstructive airway diseases. To understand these mechanisms, we measured acid‐induced mucin secretion in human bronchial epithelial cells. In the present study, acid induced inward currents of transient receptor potential vanilloid (TRPV)1 and mucin 5AC (MUC5AC) secretion dose dependently, which were inhibited by TRPV1 antagonist capsazepine in a concentration‐dependent manner. TRPV1 agonist capsaicin mediated a concentration‐dependent increase in TRPV1 inward currents and MUC5AC secretion. Furthermore, capsaicin enhanced acid‐induced TRPV1 inward currents and MUC5AC secretion. Acid‐induced Ca2+ influx was prevented by capsazepine dose dependently and enhanced by capsaicin. Pretreatment only with capsaicin also increased the Ca2+ concentration in a concentration‐dependent manner. These data suggest that pharmacological inhibition of calcium‐permeable TRPV1 receptors could be used to prevent acid‐induced mucin secretion, thereby providing a potential mechanism to reduce their toxicity. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:179–186, 2012; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.20413</div></front></TEI><affiliations><list><country><li>Niger</li><li>Russie</li><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yu, Hongmei" sort="Yu, Hongmei" uniqKey="Yu H" first="Hongmei" last="Yu">Hongmei Yu</name></noRegion><name sortKey="Li, Qi" sort="Li, Qi" uniqKey="Li Q" first="Qi" last="Li">Qi Li</name><name sortKey="Zhou, Xiangdong" sort="Zhou, Xiangdong" uniqKey="Zhou X" first="Xiangdong" last="Zhou">Xiangdong Zhou</name><name sortKey="Zhou, Xiangdong" sort="Zhou, Xiangdong" uniqKey="Zhou X" first="Xiangdong" last="Zhou">Xiangdong Zhou</name></country><country name="Niger"><noRegion><name sortKey="Zhou, Xiangdong" sort="Zhou, Xiangdong" uniqKey="Zhou X" first="Xiangdong" last="Zhou">Xiangdong Zhou</name></noRegion></country><country name="Russie"><noRegion><name sortKey="Kolosov, Victor P" sort="Kolosov, Victor P" uniqKey="Kolosov V" first="Victor P." last="Kolosov">Victor P. Kolosov</name></noRegion><name sortKey="Perelman, Juliy M" sort="Perelman, Juliy M" uniqKey="Perelman J" first="Juliy M." last="Perelman">Juliy M. Perelman</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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