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doi: 10.1242/10.1242/jcs.00627
Research Article |
1 Department of Medicine, Mayo Clinic Rochester, Rochester, MN 55905, USA
2 Department of Immunology, Mayo Clinic Rochester, Rochester, MN 55905,
USA
3 Department of Dermatology, University of Utah, Salt Lake City, UT 84132,
USA
4 Department of Physiology, University of Minnesota, St Paul, MN 55108,
USA
5 Department of Animal Science, University of Minnesota, St Paul, MN 55108,
USA
* Author for correspondence (e-mail: bankers.jennifer{at}mayo.edu)
Accepted 22 April 2003
Protein kinase C (PKC) activation in human eosinophils increases NADPH
oxidase activity, which is associated with plasma membrane depolarization. In
this study, membrane potential measurements of eosinophils stimulated with
phorbol ester (phorbol 12-myristate 13-acetate; PMA) were made using a
cell-permeable oxonol membrane potential indicator, diBAC4(3).
Within 10 minutes after PMA stimulation, eosinophils depolarized from
–32.9±5.7 mV to +17.3±1.8 mV. The time courses of
depolarization and proton channel activation were virtually identical.
Blocking the proton conductance with 250 µM ZnCl2
(+43.0±4.2 mV) or increasing the proton channel activation threshold by
reducing the extracellular pH to 6.5 (+44.4±1.4 mV) increased
depolarization compared with PMA alone. Additionally, the protein kinase C
(PKC) 
-selective blocker, rottlerin, inhibited PMA-stimulated
depolarization, indicating that PKC was involved in regulating
depolarization associated with eosinophil NADPH oxidase activity. Thus, the
membrane depolarization that is associated with NADPH oxidase activation in
eosinophils is sufficient to produce marked proton channel activation under
physiological conditions.
Key words: Membrane potential, PKC, superoxide, H+ channel, NADPH oxidase
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