Evidence map›Paper›PMID 25545365›Full record

ArticleThe Journal of physiology2015

Wnt signalling suppresses voltage-dependent Na⁺ channel expression in postnatal rat cardiomyocytes.

Wenbin Liang, Hee Cheol Cho, Eduardo Marbán

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 18% 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, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Genome Editing and Inherited Cardiac Arrhythmias.Advances in experimental medicine and biology · 2023
    Article
  6. Article
  7. Review
  8. Glycogen Synthase Kinase 3: Ion Channels, Plasticity, and Diseases.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. A small-molecule LF3 abrogates β-catenin/TCF4-mediated suppression of NaJournal of molecular and cellular cardiology · 2019
    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

3 authors at 2 institutions in 1 country.

Wenbin LiangCedars-Sinai Heart Institute, Los Angeles, CA, USA.
Hee Cheol Cho
Eduardo Marbán
Cedars-Sinai Smidt Heart Institute · USEmory University · US

Funding

Molecular determinants of the cardiac pacemaker automaticityR01HL111646 · NHLBI · EMORY UNIVERSITY · PI CHO, HEE CHEOL · 2012 to 2016
$2.0M
Canadian Institutes of Health ResearchNHLBI NIH HHS 1R01HL111646-01A1NHLBI NIH HHS R01 HL111646
6 · The paper itself

Abstract

Wnt signalling plays crucial roles in heart development, but is normally suppressed postnatally. In arrhythmogenic conditions, such as cardiac hypertrophy and heart failure, Wnt signalling is reactivated. To explore the potential role of Wnt signalling in arrhythmogenic electrical remodelling, we examined voltage-dependent ion channels in cardiomyocytes. Treatment of neonatal rat ventricular myocytes with either recombinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3β inhibitor) caused a dose-dependent increase in Wnt target gene expression (Axin2 and Lef1), indicating activation of the Wnt/β-catenin pathway. Cardiac Na(+) current (INa) density was reduced by Wnt3a (-20 ± 4 vs. control -59 ± 7 pA pF(-1) , at -30 mV) or CHIR (-22 ± 5 pA pF(-1) ), without changes in steady-state activation, inactivation or repriming kinetics. Wnt3a and CHIR also produced dose-dependent reductions in the mRNA level of Scn5a (the cardiac Na(+) channel α subunit gene), as well as a 56% reduction (by Wnt3a) in the Nav 1.5 protein level. Consistent with INa reduction, action potentials in Wnt3a-treated neonatal rat ventricular myocytes had a lower upstroke amplitude (91 ± 3 vs. control 137 ± 2 mV) and decreased maximum upstroke velocity (70 ± 10 vs. control 163 ± 15 V s(-1)). In contrast, inward rectifier K(+) current and L-type Ca(2+) channels were not affected by Wnt3a treatment. Taken together, our data indicate that the Wnt/β-catenin pathway suppresses INa in postnatal cardiomyocytes and may contribute to ion channel remodelling in heart disease.

Indexed as

Wnt Signaling PathwayAction PotentialsAdaptor Proteins, Signal TransducingAnimalsCalcium Channels, L-TypeCarrier ProteinsCells, CulturedGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaLymphoid Enhancer-Binding Factor 1Myocytes, CardiacNAV1.5 Voltage-Gated Sodium ChannelPotassium Channels, Inwardly RectifyingRatsRats, Sprague-DawleyWnt3A ProteinAdaptor Proteins, Signal TransducingAxin2 protein, ratCalcium Channels, L-TypeCarrier ProteinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratLef1 protein, ratLymphoid Enhancer-Binding Factor 1NAV1.5 Voltage-Gated Sodium ChannelPotassium Channels, Inwardly RectifyingScn5a protein, ratWnt3A Protein

Identifiers

PMID25545365
PMCPMC4358676
OpenAlexW2166946152

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.