Most basal isc in calu-3 human airway cells is bicarbonate
dependent cl secretion.
Singh, Meetpaul, Mauri Krouse, Samina Moon, and Jeffrey J. Wine.
Cystic Fibrosis Research Laboratory, Stanford University, Stanford,
CA 94305-2130
APStracts 3:0216L, 1996.
Serous cells secrete antibiotic_rich fluid, but secretion is impaired
in cystic fibrosis. We are investigating Calu-3 cells as a serous
cell model. Basal Isc in Calu-3 cells grown at air interface had a
basal Isc 6 times larger than submerged cultures (69 +/- 22 vs. 11
+/- 10 [mu]A/cm2). Basal Isc in either condition was reduced only 7
+/- 5 % by bumetanide and was unaffected by apical amiloride, DIDS,
DNDS, or Calixarene, but was reduced 77 +/- 18% by DPAC. Three
transport mechanisms accounted for almost all basal Isc. The largest
component is HCO3--dependent Cl- secretion. Replacement of Krebs
-Henseleit solution with HEPES-buffered solution and changing gassing
from 95% O2/5% CO2 to air reduced the basal Isc by 61 +/- 10%.
Acetazolamide decreased basal Isc by 33 +/- 6% while acetazolamide
& basolateral DNDS eliminated 42-58% of the
bumetanide_insensitive basal Isc. Neither DNDS nor acetazolamide had
any effect when applied in HCO3-_free solution. Apical phlorizin, a
blocker of Na&/glucose transport, eliminated half of the
remaining Isc. Cl- replacement with gluconate eliminated all Isc
except the phlorizin-sensitive component. Unlike basal Isc, 80 +/- 24
% of stimulated Isc was inhibited by bumetanide. Thus, basal and
stimulated secretions are mediated by different mechanisms.
Received 17 July 1996; accepted in final form 6 November 1996.
APS Manuscript Number L226-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996