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[$Ca^{2+}$ Signalling in Endothelial Cells: Role of Ion Channels

Nilius, Bernd   (KU Leuven, Campus Gasthuisberg, Department of Physiology  ); Viana, Felix   (KU Leuven, Campus Gasthuisberg, Department of Physiology  ); Kamouchi, Masahiro   (KU Leuven, Campus Gasthuisberg, Department of Physiology  ); Fasolato, Cristina   (KU Leuven, Campus Gasthuisberg, Department of Physiology  ); Eggermont, Jan   (KU Leuven, Campus Gasthuisberg, Department of Physiology  ); Droogmans, Guy   (KU Leuven, Campus Gasthuisberg, Department of Physiology  );
  • 초록

    $Ca^{2+}-signals$ in endothelial cells are determined by release from intracellular stores and entry through the plasma membrane. In this review, the nature of $Ca^{2+}$ entry and mechanisms of its control are reviewed. The following ion channels play a pivotal role in regulation of the driving force for $Ca^{2+}$ entry: an inwardly rectifying $K^+$ channel, identified as Kir2.1, a big-conductance, $Ca^{2+}-activated$ $K^+$ channel (hslo) and at least two $Cl^-$ channels (a volume regulated $Cl^-$ channel, VRAC, and a $Ca^{2+}$ activated $Cl^-$ channel, CaCC). At least two different types of $Ca^{2+}$ -entry channels exist: 1. A typical CRAC-like, highly selective $Ca^{2+}$ channel is described. Current density for this $Ca^{2+}$ entry is approximately 0.1pA/pF at 0 mV and thus 10 times smaller than in Jurkat or mast cells. 2. Another entry pathway for $Ca^{2+}$ entry is a more non-selective channel, which might be regulated by intracellular $Ca^{2+}$ . Although detected in endothelial cells, the functional role of trp1,3,4 as possible channel proteins is unclear. Expression of trp3 in macrovascular endothelial cells from bovine pulmonary artery induced non-selective cation channels which are probably not store operated or failed to induce any current. Several features as well as a characterisation of $Ca^{2+}$ -oscillations in endothelial cells is also presented.


  • 주제어

    Endothelium- $Ca^{2+}$-entry channels-potassium channels- $Ca^{2+}$-oscillations.  

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