A molecular study on the endoplasmic reticulum potassium channels in hepatocytes

Authors

  • Afsaneh Eliassi Dept. of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Iran
  • Fariba Khodagholi Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Iran
  • Maedeh Ghasemi Dept. of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Iran
  • Naser Khodaee ataloo Dept. of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Iran
Abstract:

Introduction: It has recently been suggested that the KATP channel subunits Kir6.x and BKCa channels exist in the endoplasmic reticulum of cardiomyocytes and neurons. Our previous studies showed the electrophysiological behavior of cation channels in the rough endoplasmic reticulum (RER) of rat hepatocytes. Therefore, we hypothesized that KATP channels and Ca2+-activated potassium channels may exist in RER of the liver. Methods: Ion channel incorporation of RER of hepatocytes into the bilayer lipid membrane and western blotting allowed the identification of the rerKATP and Ca2+-activated potassium channels of intermediate conductance (rerIKCa channel). Results: Single channel recordings revealed a 211 pS K channel, which was sensitive to 200 nM charibdotoxin. In addition, adding 2.5 mM ATP, 100 μM glibenclamide and 400 μM tolbutamide inhibited a 596 pS potassium channel activity. According to the results of western blot analysis, Kir6.2, SUR1 and/or SUR2B, SUR2A and IKCa were expressed in the endoplasmic reticulum fractions. Conclusion: The data obtained in this study demonstrate, in part, the composition of rerKATP channel and the presence of rerIKCa in the endoplasmic reticulum of the liver. These results will be useful for further analysis of the composition of rerKATP and rerIKCa channels and help to understand the role of these channels in diseases.

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Journal title

volume 18  issue None

pages  304- 314

publication date 2014-10

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