β 2 adrenoceptor signaling regulates ion transport in 16HBE14o- human airway epithelial cells.

Autor: Zhang RG; Department of Physiology, Basic Medical School, Guangdong Medical University, China., Yip CY; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China., Pan KW; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China., Cai MY; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China., Ko WH; School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Jazyk: angličtina
Zdroj: Journal of cellular physiology [J Cell Physiol] 2020 Nov; Vol. 235 (11), pp. 8387-8401. Date of Electronic Publication: 2020 Apr 02.
DOI: 10.1002/jcp.29683
Abstrakt: 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.
(© 2020 Wiley Periodicals, Inc.)
Databáze: MEDLINE
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