Evidence map›Paper›PMID 21224218›Full record

ArticleThe Journal of physiology2011

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

Kevin Monaghan, Salah A Baker, Laura Dwyer, William C Hatton, Kyung Sik Park, Kenton M Sanders, Sang Don Koh

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  3. Vascular mechanotransduction.Physiological reviews · 2023
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  17. Myometrial relaxation of mice via expression of two pore domain acid sensitive K(+) (TASK-2) channels.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kevin MonaghanDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.
Salah A Baker
Laura Dwyer
William C Hatton
Kyung Sik Park
Kenton M Sanders
Sang Don Koh
University of Nevada, Reno · US

Funding

STRETCH DEPENDENT POTASSIUM CHANNEL REGULATION IN OVERACTIVE BLADDERP20RR018751 · NCRR · UNIVERSITY OF NEVADA RENO · PI KOH, SANG DON · 2003 to 2011
$17.3M
Functional and molecular identification of TREK-1 channel in myometrium in relatiR21HD060077 · NICHD · UNIVERSITY OF NEVADA RENO · PI KOH, SANG DON · 2009 to 2010
$351k
NCRR NIH HHS 5P20-RR018751NCRR NIH HHS P20 RR018751NICHD NIH HHS R21 HD060077NICHD NIH HHS R21HD060077
6 · The paper itself

Abstract

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 Ca2+. 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.

Indexed as

AnimalsBlotting, WesternDown-RegulationFemaleImmunohistochemistryMembrane PotentialsMiceMicroelectrodesMuscle ContractionMuscle, SmoothMyocytes, Smooth MuscleMyometriumOvariectomyParturitionPatch-Clamp TechniquesPotassium Channels, Tandem Pore Domainpotassium channel protein TREK-1Potassium Channels, Tandem Pore DomainRNA, Messenger

Identifiers

PMID21224218
PMCPMC3060598
OpenAlexW1533225373

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.