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Functional expression of TREK-2 in insulin-secreting MIN6 cells.

Abstract：

:Insulin secretion from pancreatic beta cells is partly regulated by cell membrane potential. Background K+ channels that stabilize the resting membrane potential would suppress excitability and insulin secretion. Recent studies show that members of the two-pore domain K+ (K2P) channel family behave as background K+ channels in many excitable cells. Therefore, the expression of K2P channels was studied in insulin-secreting MIN6 cells. Reverse transcriptase PCR showed that, among nine K2P channels tested, TASK-1, TASK-2, TASK-3, TREK-2, and TRESK-2 were expressed in MIN6 cells. Cell-attached recordings on MIN6 cells revealed five types of K+ channels that were open at rest. Two were ATP-sensitive and Ca2+-activated K+ channels, as judged by their sensitivity to ATP and Ca2+, respectively, and single-channel conductance. Among five K2P channels, only TREK-2 could be clearly identified in MIN6 cells. The molecular identity of two other K+ channels is not yet known. TREK-2 in MIN6 cells was activated by arachidonic acid, membrane stretch, and low pH solution (pH 5.8). Arachidonic acid increased Ba2+-sensitive whole-cell current in MIN6 cell. These results suggest that TREK-2 contributes to the background K+ conductance in MIN6 cells, and may regulate depolarization-induced secretion of insulin.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kang D,Choe C,Kim D

doi

10.1016/j.bbrc.2004.08.089

subject

Has Abstract

pub_date

2004-10-08 00:00:00

pages

323-31

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(04)01823-6

journal_volume

323

pub_type

杂志文章

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