Evidence map›Paper›PMID 18305226›Full record

ArticleBiology of reproduction2008

Overexpression of SK3 channels dampens uterine contractility to prevent preterm labor in mice.

Stephanie L Pierce, Jessica D K Kresowik, Kathryn G Lamping, Sarah K England

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Developmental and mechanical roles of Reichert's membrane in mouse embryos.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  4. Review
  5. Article
  6. Augmented KInternational journal of molecular sciences · 2021
    Article
  7. Uterine contractions in rodent models and humans.Acta physiologica (Oxford, England) · 2021
    Review
  8. Article
  9. Tocolysis: Present and future treatment options.Seminars in perinatology · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Transforming growth factor β signaling in uterine development and function.Journal of animal science and biotechnology · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Stephanie L PierceDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA 52242, USA.
Jessica D K Kresowik
Kathryn G Lamping
Sarah K England
University of Iowa · US

Funding

REGULATION OF UTERINE SMOOTH MUSCLE EXCITABILITYR01HD037831 · NICHD · WASHINGTON UNIVERSITY · PI ENGLAND, SARAH K. · 1999 to 2023
$7.0M
NICHD NIH HHS HD-037831NICHD NIH HHS R01 HD037831
6 · The paper itself

Abstract

The mechanisms that control the timing of labor have yet to be fully characterized. In a previous study, the overexpression of small conductance calcium-activated K(+) channel isoform 3 in transgenic mice, Kcnn3(tm1Jpad)/Kcnn3(tm1Jpad) (also known as SK3(T/T)), led to compromised parturition, which indicates that KCNN3 (also known as SK3) plays an important role in the delivery process. Based on these findings, we hypothesized that SK3 channel expression must be downregulated late in pregnancy to enable the uterus to produce the forceful contractions required for parturition. Thus, we investigated the effects of SK3 channel expression on gestation and parturition, comparing SK3(T/T) mice to wild type (WT) mice. Here, we show in WT mice that SK3 transcript and protein are significantly reduced during pregnancy. We also found the force produced by uterine strips from Pregnancy Day 19 (P19) SK3(T/T) mice was significantly less than that measured in WT or SK3 knockout control (SK3(DOX)) uterine strips, and this effect was reversed by application of the SK3 channel inhibitor apamin. Moreover, two treatments that induce labor in mice failed to result in complete delivery in SK3(T/T) mice within 48 h after injection. Thus, stimuli that initiate parturition under normal circumstances are insufficient to coordinate the uterine contractions needed for the completion of delivery when SK3 channel activity is in excess. Our data indicate that SK3 channels must be downregulated for the gravid uterus to generate labor contractions sufficient for delivery in both term and preterm mice.

Indexed as

AnimalsBase SequenceDNA, ComplementaryDown-RegulationFemaleGene ExpressionMiceMice, Inbred C57BLMice, TransgenicMyometriumObstetric Labor, PrematurePregnancySmall-Conductance Calcium-Activated Potassium ChannelsUterine ContractionDNA, ComplementaryKcnn3 protein, mouseSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID18305226
PMCPMC2930016
OpenAlexW2169484885

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.