PKA and arachidonic acid activation of human recombinant ClC-2 chloride channels |
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Authors: | Tewari K P Malinowska D H Sherry A M Cuppoletti J |
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Affiliation: | Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0576, USA. |
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Abstract: | An HEK-293 cell line stably expressing the humanrecombinant ClC-2 Cl channel was used in patch-clampstudies to study its regulation. The relative permeabilityPx/PCl calculated fromreversal potentials was I > Cl = NO3 = SCN![-](http://ajpcell.physiology.org/math/12pt/normal/scr/minus.gif) Br . Theabsolute permeability calculated from conductance ratios wasCl = Br = NO3 SCN > I . The channel was activatedby cAMP-dependent protein kinase (PKA), reduced extracellular pH, oleicacid (C:18 cis 9), elaidic acid (C:18trans 9), arachidonic acid (AA; C:20cis 5,8,11,14), and by inhibitors of AA metabolism,5,8,11,14-eicosatetraynoic acid (ETYA; C:20trans 5,8,11,14), -methyl-4-(2-methylpropyl)benzeneacetic acid (ibuprofen), and2-phenyl-1,2-benzisoselenazol-3-[2H]-one (PZ51, ebselen). ClC-2Cl channels were activated by a combination of forskolinplus IBMX and were inhibited by the cell-permeant myristoylated PKAinhibitor (mPKI). Channel activation by reduction of bath pH wasincreased by PKA and prevented by mPKI. AA activation of the ClC-2Cl channel was not inhibited by mPKI or staurosporine andwas therefore independent of PKA or protein kinase C activation. |
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