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This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/C611    most recent 00435.2007v1 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 HighWire Google Scholar Articles by Layne, J. Articles by Nelson, M. PubMed PubMed Citation Articles by Layne, J. Articles by Nelson, M.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

NFATc3 regulates BK channel function in murine urinary bladder smooth muscle

¹Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont; and ²Division of Cardiovascular and Endocrine Science, School of Medicine, University of Manchester, Manchester, United Kingdom

Submitted 21 September 2007 ; accepted in final form 22 June 2008

The nuclear factor of activated T-cells (NFAT) is a Ca²⁺-dependent transcription factor that has been reported to regulate the expression of smooth muscle contractile proteins and ion channels. Here we report that large conductance Ca²⁺-sensitive potassium (BK) channels and voltage-gated K⁺ (K_V) channels may be regulatory targets of NFATc3 in urinary bladder smooth muscle (UBSM). UBSM myocytes from NFATc3-null mice displayed a reduction in iberiotoxin (IBTX)-sensitive BK currents, a decrease in mRNA for the pore-forming -subunit of the BK channel, and a reduction in BK channel density compared with myocytes from wild-type mice. Tetraethylammonium chloride-sensitive K_V currents were elevated in UBSM myocytes from NFATc3-null mice, as was mRNA for the Shab family member K_V2.1. Despite K_V current upregulation, bladder strips from NFATc3-null mice displayed an elevated contractile response to electrical field stimulation relative to strips from wild-type mice, but this difference was abrogated in the presence of the BK channel blocker IBTX. These results support a role for the transcription factor NFATc3 in regulating UBSM contractility, primarily through an NFATc3-dependent increase in BK channel activity.

large conductance potassium channel; voltage-gated potassium; nuclear factor of activated T-cell; contractility; urinary bladder

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