## Abstract Hyperglycemia, a symptom of diabetes mellitus, induces hyperosmotic responses, including apoptosis, in vascular endothelial cells and leukocytes. Hyperosmotic shock elicits a stress response in mammalian cells, often leading to apoptotic cell death. In a previous report, we showed that
Properties of Mg2+-dependent cation channels in human leukemia K562 cells
✍ Scribed by Svetlana B. Semenova; Alla F. Fomina; Irina O. Vassilieva; Yuri A. Negulyaev
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 154 KB
- Volume
- 205
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The endogenous Mg^2+^‐inhibited cation (MIC) current was recently described in different cells of hematopoietic lineage and was implicated in the regulation of Mg^2+^ homeostasis. Here we present a single channel study of endogenously expressed Mg^2+^‐dependent cation channels in the human myeloid leukemia K562 cells. Inwardly directed unitary currents were activated in cell‐attached experiments in the absence of Ca^2+^ and Mg^2+^ in the pipette solution. The current–voltage (I–V) relationships displayed strong inward rectification and yielded a single channel slope conductance of ∼30 pS at negative potentials. The I–V relationships were not altered by patch excision into divalent‐free solution. Channel open probability (P~o~) and mean closed time constant (τ~C~) were strongly voltage‐dependent, indicating that gating mechanisms may underlie current inward rectification. Millimolar concentrations of Ca^2+^ or Mg^2+^ applied to the cytoplasmic side of the membrane produced slow irreversible inhibition of channel activity. The Mg^2+^‐dependent cation channels described in this study differ from the MIC channels described in human T‐cells, Jurkat, and rat basophilic leukemia (RBL) cells in their I–V relationships, kinetic parameters and dependence on intracellular divalent cations. Our results suggested that endogenously expressed Mg^2+^‐dependent cation channels in K562 cells and the MIC channels in other hematopoietic cells might be formed by different channel proteins. © 2005 Wiley‐Liss, Inc.
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