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β 2 adrenoceptor signaling regulates ion transport in 16HBE14o‐ human airway epithelial cells
Author(s) -
Zhang RuiGang,
Yip ChungYin,
Pan Kewu,
Cai Mengyun,
Ko WingHung
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29683
Subject(s) - cystic fibrosis transmembrane conductance regulator , isoprenaline , intracellular , endocrinology , medicine , agonist , chloride channel , cyclic adenosine monophosphate , chemistry , adenosine , secretion , propranolol , microbiology and biotechnology , signal transduction , receptor , biology , cystic fibrosis , stimulation
We investigated the regulation of Cl − secretion by adrenoceptors in polarized 16HBE14o‐ human bronchial epithelial cells. Treatment with the nonselective β adrenoceptor agonist isoprenaline stimulated an increase in short‐circuit current ( I SC ), which was inhibited by the β adrenoceptor blocker propranolol. Treatment with procaterol, an agonist specific for the β 2 adrenoceptor subtype, stimulated a similar increase in I SC , which was inhibited by the β 2 adrenoceptor antagonist ICI 118551. Inhibitors of cystic fibrosis transmembrane conductance regulator (CFTR) and calcium‐activated Cl − channel (CaCC), but not K + channel blockers, were able to inhibit the increase in I SC . “Trimultaneous” recording of I SC and intracellular cyclic adenosine monophosphate (cAMP) and Ca 2+ levels in 16HBE14o‐ epithelia confirmed that the I SC induced by isoprenaline or procaterol involved both cAMP and Ca 2+ signaling. Our results demonstrate that β 2 adrenoceptors regulate Cl − secretion in the human airway epithelium by activating apical CFTRs and CaCCs via cAMP‐dependent and intracellular Ca 2+ ‐dependent mechanisms, respectively.