Evidence map›Paper›PMID 29543863›Full record

ArticlePloS one2018

Distinct transcriptomic changes in E14.5 mouse skeletal muscle lacking RYR1 or Cav1.1 converge at E18.5.

Dilyana Filipova, Margit Henry, Tamara Rotshteyn, Anna Brunn, Mariana Carstov, Martina Deckert, Jürgen Hescheler, Agapios Sachinidis, Gabriele Pfitzer, Symeon Papadopoulos

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 22 citations in OpenAlex.

  1. Biomolecules · 2025
    Article
  2. Article
  3. Ryanodine receptor RyR1-mediated elevation of CaJournal of animal science and biotechnology · 2022
    Article
  4. Article
  5. Article
  6. 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

10 authors at 1 institution in 1 country.

Dilyana FilipovaInstitute of Vegetative Physiology, Center of Physiology and Pathophysiology, University of Cologne, Cologne, Germany.ORCID 0000-0003-3532-9765
Margit HenryInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Tamara RotshteynInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Anna BrunnDepartment of Neuropathology, University of Cologne, Cologne, Germany.
Mariana CarstovDepartment of Neuropathology, University of Cologne, Cologne, Germany.
Martina DeckertDepartment of Neuropathology, University of Cologne, Cologne, Germany.
Jürgen HeschelerInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Agapios SachinidisInstitute of Neurophysiology and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Gabriele PfitzerInstitute of Vegetative Physiology, Center of Physiology and Pathophysiology, University of Cologne, Cologne, Germany.
Symeon PapadopoulosInstitute of Vegetative Physiology, Center of Physiology and Pathophysiology, University of Cologne, Cologne, Germany.ORCID 0000-0002-0708-7431
University of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In skeletal muscle the coordinated actions of two mechanically coupled Ca2+ channels-the 1,4-dihydropyridine receptor (Cav1.1) and the type 1 ryanodine receptor (RYR1)-underlie the molecular mechanism of rapid cytosolic [Ca2+] increase leading to contraction. While both [Ca2+]i and contractile activity have been implicated in the regulation of myogenesis, less is known about potential specific roles of Cav1.1 and RYR1 in skeletal muscle development. In this study, we analyzed the histology and the transcriptomic changes occurring at E14.5 -the end of primary myogenesis and around the onset of intrauterine limb movement, and at E18.5 -the end of secondary myogenesis, in WT, RYR1-/-, and Cav1.1-/- murine limb skeletal muscle. At E14.5 the muscle histology of both mutants exhibited initial alterations, which became much more severe at E18.5. Immunohistological analysis also revealed higher levels of activated caspase-3 in the Cav1.1-/- muscles at E14.5, indicating an increase in apoptosis. With WT littermates as controls, microarray analyses identified 61 and 97 differentially regulated genes (DEGs) at E14.5, and 493 and 1047 DEGs at E18.5, in RYR1-/- and Cav1.1-/- samples, respectively. Gene enrichment analysis detected no overlap in the affected biological processes and pathways in the two mutants at E14.5, whereas at E18.5 there was a significant overlap of DEGs in both mutants, affecting predominantly processes linked to muscle contraction. Moreover, the E18.5 vs. E14.5 comparison revealed multiple genotype-specific DEGs involved in contraction, cell cycle and miRNA-mediated signaling in WT, neuronal and bone development in RYR1-/-, and lipid metabolism in Cav1.1-/- samples. Taken together, our study reveals discrete changes in the global transcriptome occurring in limb skeletal muscle from E14.5 to E18.5 in WT, RYR1-/- and Cav1.1-/- mice. Our results suggest distinct functional roles for RYR1 and Cav1.1 in skeletal primary and secondary myogenesis.

Indexed as

Gene Expression Regulation, DevelopmentalTranscriptomeAnimalsCalcium Channels, L-TypeGene OntologyHindlimbMice, Inbred C57BLMice, KnockoutMuscle DevelopmentMuscle, SkeletalRyanodine Receptor Calcium Release ChannelTime FactorsCACNA1S protein, mouseCalcium Channels, L-Typeryanodine receptor 1, mouseRyanodine Receptor Calcium Release Channel

Identifiers

PMID29543863
PMCPMC5854361
OpenAlexW2792992676

What OpenQuestion holds

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LicenceCC BY
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.