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Transient receptor potential vanilloid 1 receptors mediate acid‐induced mucin secretion via Ca 2+ influx in human airway epithelial cells
Author(s) -
Yu Hongmei,
Li Qi,
Zhou Xiangdong,
Kolosov Victor P.,
Perelman Juliy M.
Publication year - 2012
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.20413
Subject(s) - capsazepine , trpv1 , capsaicin , mucin , transient receptor potential channel , chemistry , secretion , trpv , receptor , medicine , endocrinology , pharmacology , biochemistry , biology
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 Ca 2+ influx was prevented by capsazepine dose dependently and enhanced by capsaicin. Pretreatment only with capsaicin also increased the Ca 2+ 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