Abstract
Voltage-Activated Ion Channels in Non-excitable Cells-A Viewpoint Regarding Their Physiological Justification.
Highlights
Reviewed by: Agnieszka Zdzisława Robaszkiewicz, University of Łódz, Poland Marta Gaburjakova, Institute of Molecular Physiology and Genetics (SAS), Slovakia
In an investigation based on comparative physiology, it became evident that the low ionic strengthinduced cation permeability in red blood cells (RBCs) is not due to electrodiffusion but due to a transport proteinbased process (Halperin et al, 1990; Bernhardt et al, 1991)
Evidence for the existence of a number of voltage-activated Ca2+ channels that are abundant in RBCs has been reported (Pinet et al, 2002; Romero et al, 2006), and the most convincing evidence is for CaV2.1, based on molecular biology data (Western blot) (Andrews et al, 2002) and, presumably, CaV2.1-specific pharmacological interactions (ω-agatoxinTK) (Andrews et al, 2002; Wagner-Britz et al, 2013)
Summary
RBCs are undoubtedly non-excitable cells, sudden changes in membrane potential occur, when increased cation permeability is induced. The physiological function of the Gardos channel remained elusive for decades, until it was discovered that it is a major component of the suicidal process of RBCs (Kaestner and Bernhardt, 2002; Lang et al, 2003; Bogdanova et al, 2013) triggered by Ca2+ entry (Yang et al, 2000; Kaestner et al, 2004), resulting in cell shrinkage (Begenisich et al, 2004; Lew et al, 2005), and phosphatidylserine exposure (Chung et al, 2007; Nguyen et al, 2011).
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