NDLI: Expression and Function of Pancreatic β-Cell Delayed Rectifier K+ Channels ROLE IN STIMULUS-SECRETION COUPLING

Content Provider	Journal of Biological Chemistry (JBC)
Author	Roe, Michael Wm Iii, Jennings F. Worley Mittal, Anshu A. Kuznetsov, Andrey DasGupta, Sarmila Mertz, Robert J. Iii, Sam M. Witherspoon Blair, Nathaniel Lancaster, Mary E. McIntyre, Margaret S. Shehee, W. Ronald Dukes, Iain D. Philipson, Louis H. Worley, Jennings F. Witherspoon, Sam M.
Abstract	Voltage-dependent delayed rectifier K+ channels regulate aspects of both stimulus-secretion and excitation-contraction coupling, but assigning specific roles to these channels has proved problematic. Using transgenically derived insulinoma cells (βTC3-neo) and β-cells purified from rodent pancreatic islets of Langerhans, we studied the expression and role of delayed rectifiers in glucose-stimulated insulin secretion. Using reverse-transcription polymerase chain reaction methods to amplify all known candidate delayed rectifier transcripts, the expression of the K+ channel gene Kv2.1 in βTC3-neo insulinoma cells and purified rodent pancreatic β-cells was detected and confirmed by immunoblotting in the insulinoma cells. βTC3-neo cells were also found to express a related K+ channel, Kv3.2. Whole-cell patch clamp demonstrated the presence of delayed rectifier K+ currents inhibited by tetraethylammonium (TEA) and 4-aminopyridine, with similar Kd values to that of Kv2.1, correlating delayed rectifier gene expression with the K+ currents. The effect of these blockers on intracellular Ca2+ concentration ([Ca2+]i) was studied with fura-2 microspectrofluorimetry and imaging techniques. In the absence of glucose, exposure to TEA (1-20 mM) had minimal effects on βTC3-neo or rodent islet [Ca2+]i, but in the presence of glucose, TEA activated large amplitude [Ca2+]i oscillations. In the insulinoma cells the TEA-induced [Ca2+]i oscillations were driven by synchronous oscillations in membrane potential, resulting in a 4-fold potentiation of insulin secretion. Activation of specific delayed rectifier K+ channels can therefore suppress stimulus-secretion coupling by damping oscillations in membrane potential and [Ca2+]i and thereby regulate secretion. These studies implicate previously uncharacterized β-cell delayed rectifier K+ channels in the regulation of membrane repolarization, [Ca2+]i, and insulin secretion.
Related Links	http://www.jbc.org/content/271/50/32241.abstract
Ending Page	32246
Starting Page	32241
Page Count	6
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	50
Volume Number	271
DOI	10.1074/jbc.271.50.32241
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	1996-12-13
Access Restriction	Open
Subject Keyword	Cell Biology and Metabolism
Alternative Title	Expression and Function of Pancreatic β-Cell Delayed Rectifier K+ Channels
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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