Literature DB >> 10191357

Cystic fibrosis transmembrane conductance regulator (CFTR) confers glibenclamide sensitivity to outwardly rectifying chloride channel (ORCC) in Hi-5 insect cells.

M Julien1, B Verrier, M Cerutti, V Chappe, M Gola, G Devauchelle, F Becq.   

Abstract

Increasing evidence is now accumulating for the involvement of the cystic fibrosis transmembrane conductance regulator (CFTR) in the control of the outwardly rectifying chloride channel (ORCC). We have examined the sensitivity of ORCC to the sulfonylurea drug glibenclamide in Hi-5 (Trichoplusia ni) insect cells infected with recombinant baculovirus expressing either wild-type CFTR, DeltaF508-CFTR or E. coli beta galactosidase cDNA and in control cells either infected with virus alone or uninfected. Iodide efflux and single channel patch-clamp experiments confirmed that forskolin and 1-methyl-3-isobutyl xanthine (IBMX) or 7-methyl-1,3 dipropyl xanthine (DPMX) activate CFTR channels (unitary conductance: 9.1 +/- 1.6 pS) only in cells expressing CFTR. In contrast, we identified 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS)-sensitive ORCC in excised membrane patches in any of the cells studied, with similar conductance (22 +/- 2.5 pS at -80 mV; 55 +/- 4.1 pS at +80 mV) and properties. In the presence of 500 microm SITS, channel open probability (Po) of ORCC was reversibly reduced to 0.05 +/- 0.01 in CFTR-cells, to 0.07 +/- 0.02 in non-CFTR expressing cells and to 0.05 +/- 0.02 in DeltaF508-cells. In Hi-5 cells that did not express CFTR, glibenclamide failed to inhibit ORCC activity even at high concentrations (100 microm), whereas 500 microm SITS reversibly inhibited ORCC. In contrast in cells expressing CFTR or DeltaF508, glibenclamide dose dependently (IC50 = 17 microm, Hill coefficient 1.2) and reversibly inhibited ORCC. Cytoplasmic application of 100 microm glibenclamide reversibly reduced Po from 0.88 +/- 0.03 to 0.09 +/- 0.02 (wash: Po = 0.85 +/- 0.1) in CFTR cells and from 0.89 +/- 0.05 to 0.08 +/- 0.05 (wash: Po = 0.87 +/- 0.1) in DeltaF508 cells. In non-CFTR expressing cells, glibenclamide (100 microm) was without effect on Po (control: Po = 0. 89 +/- 0.09, glib.: Po = 0.86 +/- 0.02; wash: Po = 0.87 +/- 0.05). These data strongly suggest that the expression of CFTR confers glibenclamide sensitivity to the ORCC in Hi-5 cells.

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Year:  1999        PMID: 10191357     DOI: 10.1007/s002329900512

Source DB:  PubMed          Journal:  J Membr Biol        ISSN: 0022-2631            Impact factor:   1.843


  5 in total

1.  The H-loop in the second nucleotide-binding domain of the cystic fibrosis transmembrane conductance regulator is required for efficient chloride channel closing.

Authors:  Monika Kloch; Michał Milewski; Ewa Nurowska; Beata Dworakowska; Garry R Cutting; Krzysztof Dołowy
Journal:  Cell Physiol Biochem       Date:  2010-01-12

Review 2.  Diversity of Cl(-) channels.

Authors:  M Suzuki; T Morita; T Iwamoto
Journal:  Cell Mol Life Sci       Date:  2006-01       Impact factor: 9.261

3.  Negative regulation of CFTR activity by extracellular ATP involves P2Y2 receptors in CFTR-expressing CHO cells.

Authors:  B Marcet; V Chappe; P Delmas; M Gola; B Verrier
Journal:  J Membr Biol       Date:  2003-07-01       Impact factor: 1.843

4.  Steady-state interactions of glibenclamide with CFTR: evidence for multiple sites in the pore.

Authors:  Z R Zhang; S Zeltwanger; N A McCarty
Journal:  J Membr Biol       Date:  2004-05-01       Impact factor: 1.843

5.  Revisiting CFTR inhibition: a comparative study of CFTRinh -172 and GlyH-101 inhibitors.

Authors:  N Melis; M Tauc; M Cougnon; S Bendahhou; S Giuliano; I Rubera; C Duranton
Journal:  Br J Pharmacol       Date:  2014-08       Impact factor: 8.739

  5 in total

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