HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 296/5/C1098    most recent 00435.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Semenova, S. B. Articles by Negulyaev, Y. A. Search for Related Content PubMed PubMed Citation Articles by Semenova, S. B. Articles by Negulyaev, Y. A.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Endogenous expression of TRPV5 and TRPV6 calcium channels in human leukemia K562 cells

¹Institute of Cytology Russian Academy of Sciences, St. Petersburg, Russia; and ²Department of Physiology and Membrane Biology, University of California, Davis, California

Submitted 22 August 2008 ; accepted in final form 23 February 2009

In blood cells, changes in intracellular Ca²⁺ concentration ([Ca²⁺]_i) are associated with multiple cellular events, including activation of cellular kinases and phosphatases, degranulation, regulation of cytoskeleton binding proteins, transcriptional control, and modulation of surface receptors. Although there is no doubt as to the significance of Ca²⁺ signaling in blood cells, there is sparse knowledge about the molecular identities of the plasmalemmal Ca²⁺ permeable channels that control Ca²⁺ fluxes across the plasma membrane and mediate changes in [Ca²⁺]_i in blood cells. Using RNA expression analysis, we have shown that human leukemia K562 cells endogenously coexpress transient receptor potential vanilloid channels type 5 (TRPV5) and type 6 (TRPV6) mRNAs. Moreover, we demonstrated that TRPV5 and TRPV6 channel proteins are present in both the total lysates and the crude membrane preparations from leukemia cells. Immunoprecipitation revealed that a physical interaction between TRPV5 and TRPV6 may take place. Single-channel patch-clamp experiments demonstrated the presence of inwardly rectifying monovalent currents that displayed kinetic characteristics of unitary TRPV5 and/or TRPV6 currents and were blocked by extracellular Ca²⁺ and ruthenium red. Taken together, our data strongly indicate that human myeloid leukemia cells coexpress functional TRPV5 and TRPV6 calcium channels that may interact with each other and contribute into intracellular Ca²⁺ signaling.

calcium ion channels; single-channel recording; blood cells; leukemia cells