Format

Send to

Choose Destination
J Physiol. 2005 Feb 1;562(Pt 3):697-706. Epub 2004 Oct 28.

Capacitative calcium entry supports calcium oscillations in human embryonic kidney cells.

Author information

1
National Institute of Environmental Health Sciences/NIH, PO Box 12233, Research Triangle Park, NC 27709, USA. bird@niehs.nih.gov

Abstract

Treatment of human epithelial kidney (HEK293) cells with low concentrations of the muscarinic agonist methacholine results in the activation of complex and repetitive cycling of intracellular calcium ([Ca(2+)](i)), known as [Ca(2+)](i) oscillations. These oscillations occur with a frequency that depends on the concentration of methacholine, whereas the magnitude of the [Ca(2+)](i) spikes does not. The oscillations do not persist in the absence of extracellular Ca(2+), leading to the conclusion that entry of Ca(2+) across the plasma membrane plays a significant role in either their initiation or maintenance. However, treatment of cells with high concentrations of GdCl(3), a condition which limits the flux of calcium ions across the plasma membrane in both directions, allows sustained [Ca(2+)](i) oscillations to occur. This suggests that the mechanisms that both initiate and regenerate [Ca(2+)](i) oscillations are intrinsic to the intracellular milieu and do not require entry of extracellular Ca(2+). This would additionally suggest that, under normal conditions, the role of calcium entry is to sustain [Ca(2+)](i) oscillations. By utilizing relatively specific pharmacological manoeuvres we provide evidence that the Ca(2+) entry that supports Ca(2+) oscillations occurs through the store-operated or capacitative calcium entry pathway. However, by artificial introduction of a non-store-operated pathway into the cells (TRPC3 channels), we find that other Ca(2+) entry mechanisms can influence oscillation frequency in addition to the store-operated channels.

Comment in

PMID:
15513935
PMCID:
PMC1665541
DOI:
10.1113/jphysiol.2004.077289
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center