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Swelling‐activated K efflux and regulatory volume decrease efficiency in human bronchial epithelial cells
Author(s) -
Caplanusi Adrian,
Kim KwangJin,
Lariviere Els,
Van Driessche Willy,
Jans Danny
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a835-c
Subject(s) - efflux , forskolin , osmotic concentration , chemistry , cell , osmotic shock , biophysics , microbiology and biotechnology , biochemistry , biology , receptor , gene
We studied the correlation between the cell swelling‐induced K efflux and regulatory volume decrease (RVD) in human bronchial epithelial cells 16HBE14o‐. Cell thickness (as an index for cell volume) and K efflux (using Rb as a substitute for K) were monitored during 30 min hyposmotic shock (by reduction of both apical and basolateral osmolality to 0.17 osmol/kg water), followed by restoration of isosmotic conditions. In control conditions, hyposmotic stress increased cell volume by 35%, with subsequent RVD restoring cell volume to 94% of isosmotic control. Subsequent exposure of cells to the isosmotic solution decreased cell volume by 33%. Basolateral Rb efflux markedly increased during hyposmotic stress (from 0.50/min to a peak 6.32/min), while apical Rb efflux was negligible during these maneuvers. Rb efflux returned to the initial value when cells were re‐exposed to isosmotic fluid. Gd, quinine, and 5‐nitro‐2‐(3‐phenyl‐propylamino) benzoic acid (NPPB) all abolished RVD, while tyrphostin 23 and genistein blocked RVD with variable degrees. Activation of adenylate cyclase by forskolin hastened the recovery of cell volume with an enhancement in K efflux. These data taken together suggest that K extrusion during RVD may be the determining factor for the efficiency of cell volume regulation in 16HBE14o‐ cells. (Supp. by HL38658, HL64365, and FWO‐V‐1.5.215.05.)