{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:21:03Z","timestamp":1772896863945,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[1997,4,1]]},"abstract":"<jats:p> 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 short-circuit current (I[SC]) in Calu-3 cells grown at air interface had a basal I(SC) approximately six times larger than submerged cultures (69 +\/- 22 vs. 11 +\/- 10 microA\/cm2). Basal I(SC) in either condition was reduced only 7 +\/- 5% by bumetanide and was unaffected by apical amiloride, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS), or calixarene but was reduced 77 +\/- 18% by N-phenylanthranilic acid. Three transport mechanisms accounted for almost all basal I(SC). The largest component is HCO3(-)-dependent Cl- secretion. Replacement of Krebs-Henseleit solution with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solution and changing gassing from 95% O2-5% CO2 to air reduced the basal I(SC) by 61 +\/- 10%. Acetazolamide decreased basal I(SC) by 33 +\/- 6%, whereas acetazolamide + basolateral DNDS eliminated 42-58% of the bumetanide-insensitive basal I(SC). Neither DNDS nor acetazolamide had any effect when applied in HCO3(-)-free solution. Apical phlorizin, a blocker of Na+-glucose cotransport, eliminated one-half of the remaining I(SC). Cl- replacement with gluconate eliminated all I(SC) except the phlorizin-sensitive component. Unlike basal I(SC), 80 +\/- 24% of stimulated I(SC) was inhibited by bumetanide. Thus basal and stimulated secretions are mediated by different mechanisms. <\/jats:p>","DOI":"10.1152\/ajplung.1997.272.4.l690","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:39:00Z","timestamp":1514036340000},"page":"L690-L698","source":"Crossref","is-referenced-by-count":19,"title":["Most basal I(SC) in Calu-3 human airway cells is bicarbonate-dependent Cl- secretion"],"prefix":"10.1152","volume":"272","author":[{"given":"M.","family":"Singh","sequence":"first","affiliation":[{"name":"Cystic Fibrosis Research Laboratory, Stanford University, California94305-2130, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Krouse","sequence":"additional","affiliation":[{"name":"Cystic Fibrosis Research Laboratory, Stanford University, California94305-2130, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Moon","sequence":"additional","affiliation":[{"name":"Cystic Fibrosis Research Laboratory, Stanford University, California94305-2130, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. J.","family":"Wine","sequence":"additional","affiliation":[{"name":"Cystic Fibrosis Research Laboratory, Stanford University, California94305-2130, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajplung.1997.272.4.L690","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:52:17Z","timestamp":1567975937000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajplung.1997.272.4.L690"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1997,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1997,4,1]]}},"alternative-id":["10.1152\/ajplung.1997.272.4.L690"],"URL":"https:\/\/doi.org\/10.1152\/ajplung.1997.272.4.l690","relation":{},"ISSN":["1040-0605","1522-1504"],"issn-type":[{"value":"1040-0605","type":"print"},{"value":"1522-1504","type":"electronic"}],"subject":[],"published":{"date-parts":[[1997,4,1]]}}}