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The stretch-dependent potassium channel TREK-1 and its function in murine myometrium

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Author(s)
Kevin MonaghanSalah A. BakerLaura DwyerWilliam C. HattonKyung Sik ParkKenton M. SandersSang Don Koh
Keimyung Author(s)
Park, Kyung Sik
Department
Dept. of Internal Medicine (내과학)
Journal Title
journal of physiology
Issued Date
2011
Volume
589
Issue
5
Abstract
Non-technical summary During pregnancy the uterus must maintain a low contractile state to
permit growth of the fetus and inhibt premature delivery. We show uterine smooth muscle cells
express specific potassium channels (called stretch-dependent potassium channels; TREK-1).
These channels are activated by stretch, stabilize resting membrane potentials of cells at negative
potentials,and reduce excitability. During pregnancy the expression of TREK-1 channels increases,
and this may contribute to reduced excitability. Near the onset of labour, TREK-1 expression
declines, and this may promote the transition to a contractile state. Thus, our data suggest
dynamic regulation of TREK-1 channel expression in the uterus contributes to the maintenance
of pregnancy.
Smooth muscle of the uterus stays remarkably quiescent during normal pregnancy
to allow sufficient time for development of the fetus. At present the mechanisms leading to
uterine quiescence during pregnancy and how the suppression of activity is relieved at term are
poorly understood. Myometrial excitability is governed by ion channels, and a major hypothesis
regarding the regulation of contractility during pregnancy has been that expression of certain
channels is regulated by hormonal influences. We have explored the expression and function
of stretch-dependent K
+
(SDK) channels, which are likely to be due to TREK channels, in
murine myometrial tissues and myocytes using PCR, Western blots, patch clamp, intracellular
microelectrode and isometric force measurements. TREK-1 is more highly expressed than
TREK-2 in myometrium, and there was no detectable expression of TRAAK. Expression of
TREK-1 transcripts and protein was regulated during pregnancy and delivery. SDK channels were
activated in response to negative pressure applied to patches. SDK channels were insensitive to a
broad-spectrum of K
+
channel blockers, including tetraethylammonium and 4-aminopyridine,
and insensitive to intracellular Ca
2+
. SDK channels were activated by stretch and arachidonic
acid and inhibited by reagents that block TREK-1 channels, L-methionine and/or methioninol.
Our data suggest that uterine excitability and contractility during pregnancy is regulated by
the expression of SDK/TREK-1 channels. Up-regulation of these channels stabilizes membrane
potential and controls contraction during pregnancy and down-regulation of these channels
induces the onset of delivery
Keimyung Author(s)(Kor)
박경식
Publisher
School of Medicine
Citation
Kevin Monaghan et al. (2011). The stretch-dependent potassium channel TREK-1 and its function in murine myometrium. journal of physiology, 589(5), 1221–1233. doi: 10.1113/jphysiol.2010.203869
Type
Article
ISSN
0022-3751
DOI
10.1113/jphysiol.2010.203869
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/34512
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Internal Medicine (내과학)
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