Evidence map›Paper›PMID 19439412›Full record

ArticleThe Journal of biological chemistry2009

Cardiotrophin-1 maintains the undifferentiated state in skeletal myoblasts.

Tetsuaki Miyake, Nezeka S Alli, Arif Aziz, Jennifer Knudson, Pasan Fernando, Lynn A Megeney, John C McDermott

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
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  19. Nuclear function of Smad7 promotes myogenesis.Molecular and cellular biology · 2010
    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

7 authors at 3 institutions in 2 countries.

Tetsuaki MiyakeDepartment of Biology, York University, Toronto, Ontario M3J 1P3, Canada.
Nezeka S Alli
Arif Aziz
Jennifer Knudson
Pasan Fernando
Lynn A Megeney
John C McDermott
York University · CAStem Cell Network · CAHealth Canada · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal myogenesis is potently regulated by the extracellular milieu of growth factors and cytokines. We observed that cardiotrophin-1 (CT-1), a member of the interleukin-6 (IL-6) family of cytokines, is a potent regulator of skeletal muscle differentiation. The normal up-regulation of myogenic marker genes, myosin heavy chain (MyHC), myogenic regulatory factors (MRFs), and myocyte enhancer factor 2s (MEF2s) were inhibited by CT-1 treatment. CT-1 also represses myogenin (MyoG) promoter activation. CT-1 activated two signaling pathways: signal transducer and activator of transcription 3 (STAT3), and mitogen-activated protein kinase kinase (MEK), a component of the extracellular signal-regulated MAPK (ERK) pathway. In view of the known connection between CT-1 and STAT3 activation, we surprisingly found that pharmacological blockade of STAT3 activity had no effect on the inhibition of myogenesis by CT-1 suggesting that STAT3 signaling is dispensable for myogenic repression. Conversely, MEK inhibition potently reversed the inhibition of myotube formation and attenuated the repression of MRF transcriptional activity mediated by CT-1. Taken together, these data indicate that CT-1 represses skeletal myogenesis through interference with MRF activity by activation of MEK/ERK signaling. In agreement with these in vitro observations, exogenous systemic expression of CT-1 mediated by adenoviral vector delivery increased the number of myonuclei in normal post-natal mouse skeletal muscle and also delayed skeletal muscle regeneration induced by cardiotoxin injection. The expression pattern of CT-1 in embryonic and post-natal skeletal muscle and in vivo effects of CT-1 on myogenesis implicate CT-1 in the maintenance of the undifferentiated state in muscle progenitor cells.

Indexed as

AnimalsBlotting, WesternButadienesCell DifferentiationCell LineCytokinesEnzyme InhibitorsFlavonoidsGene ExpressionGreen Fluorescent ProteinsImmunoprecipitationMAP Kinase Kinase 1MiceMuscle DevelopmentMuscle, SkeletalMyoblasts, Skeletal2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneButadienescardiotrophin 1CytokinesEnzyme InhibitorsFlavonoidsGreen Fluorescent ProteinsMap2k1 protein, mouseMAP Kinase Kinase 1Myogenic Regulatory FactorsMyosin Heavy ChainsNitrilesRecombinant ProteinsStat3 protein, mouseSTAT3 Transcription FactorU 0126

Identifiers

PMID19439412
PMCPMC2740593
OpenAlexW2031205775

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.