The effect of K+/H+ antiporter nigericin on gap junction permeability

Irene V. Budunova; Leonid A. Mittelman

doi:10.1007/BF00119295

The effect of K+/H+ antiporter nigericin on gap junction permeability

Irene V. Budunova^*, Leonid A. Mittelman

^*Corresponding author for this work

Dermatology

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

The K+/H+ antiporter nigericin inhibits the intercellular exchange of the fluorescent dye Lucifer Yellow between DM15-transformed fibroblasts derived from the Djungarian hamster. The efficacy of nigericin action was related to its concentration and time of incubation. The nigericin-induced uncoupling effect on gap junctions was reversible and was shown to be based on its ability to cause cystolic acidification. The effect of nigericin on dye-coupling in intact and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) pretreated cells did not differ, indicating that the uncoupling effect of H⁺ on gap junctions in DM15 cells was not mediated by the TPA-dependent isoform of protein kinase C.

Original language	English (US)
Pages (from-to)	63-73
Number of pages	11
Journal	Cell Biology and Toxicology
Volume	8
Issue number	1
DOIs	https://doi.org/10.1007/BF00119295
State	Published - Mar 1 1992

Keywords

H
gap junctions
nigericin
protein kinase C

ASJC Scopus subject areas

Toxicology
Cell Biology
Health, Toxicology and Mutagenesis

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AB - The K+/H+ antiporter nigericin inhibits the intercellular exchange of the fluorescent dye Lucifer Yellow between DM15-transformed fibroblasts derived from the Djungarian hamster. The efficacy of nigericin action was related to its concentration and time of incubation. The nigericin-induced uncoupling effect on gap junctions was reversible and was shown to be based on its ability to cause cystolic acidification. The effect of nigericin on dye-coupling in intact and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) pretreated cells did not differ, indicating that the uncoupling effect of H+ on gap junctions in DM15 cells was not mediated by the TPA-dependent isoform of protein kinase C.

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