Evidence map›Paper›PMID 19509079›Full record

ArticlePhysiological genomics2009

Skeletal muscle gene expression after myostatin knockout in mature mice.

Stephen Welle, Andrew Cardillo, Michelle Zanche, Rabi Tawil

Abstract read
In one paragraph

Article in Physiological genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Muscle Wasting and Sarcopenia in Heart Failure-The Current State of Science.International journal of molecular sciences · 2020
    Review
  4. EffectiveInternational journal of molecular sciences · 2020
    Article
  5. Article
  6. Article
  7. Methyltransferase-like 21e inhibits 26S proteasome activity to facilitate hypertrophy of type IIb myofibers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Systemic Blockade of ACVR2B Ligands Protects Myocardium from Acute Ischemia-Reperfusion Injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Pharmacology of manipulating lean body mass.Clinical and experimental pharmacology & physiology · 2015
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Effect of postdevelopmental myostatin depletion on myofibrillar protein metabolism.American journal of physiology. Endocrinology and metabolism · 2011
    Article
  19. Myostatin from the heart: local and systemic actions in cardiac failure and muscle wasting.American journal of physiology. Heart and circulatory physiology · 2011
    Review
  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.

Stephen WelleDepartment of Medicine, University of Rochester, Rochester, New York, USA. stephen_welle@urmc.rochester.edu
Andrew Cardillo
Michelle Zanche
Rabi Tawil
University of Rochester · US

Funding

UNIVERSITY OF ROCHESTER'S RESEARCH ASSOCIATE ORGANIZATIONUL1RR024160 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$38.7M
Muscle protein synthesis and gene expression in myostatin-deficient miceR01AR054366 · NIAMS · UNIVERSITY OF ROCHESTER · PI WELLE, STEPHEN L · 2007 to 2010
$1.1M
NCRR NIH HHS RR-024160NCRR NIH HHS UL1 RR024160NIAMS NIH HHS AR-054366
6 · The paper itself

Abstract

There is much interest in developing anti-myostatin agents to reverse or prevent muscle atrophy in adults, so it is important to characterize the effects of reducing myostatin activity after normal muscle development. For assessment of the effect of loss of myostatin signaling on gene expression in muscle, RNA from mice with postdevelopmental myostatin knockout was analyzed with oligonucleotide microarrays. Myostatin was undetectable in muscle within 2 wk after Cre recombinase activation in 4-month-old male mice with floxed myostatin genes. Three months after myostatin depletion, muscle mass had increased 26% (vs. 2% after induction of Cre activity in mice with normal myostatin genes), at which time the expression of several hundred genes differed in knockout and control mice at nominal P < 0.01. In contrast to previously reported effects of constitutive myostatin knockout, postdevelopmental knockout did not downregulate expression of genes encoding slow isoforms of contractile proteins or genes encoding proteins involved in energy metabolism. Several collagen genes were expressed at 20-50% lower levels in the myostatin-deficient muscles, which had approximately 25% less collagen than normal muscles as reflected by hydroxyproline content. Most of the other genes affected by myostatin depletion have not been previously linked to myostatin signaling. Gene set enrichment analysis suggested that Smads are not the only transcription factors with reduced activity after myostatin depletion. These data reinforce other evidence that myostatin regulates collagen production in muscle and demonstrate that many of the previously reported effects of constitutive myostatin deficiency do not occur when myostatin is knocked out in mature muscles.

Indexed as

Gene Expression ProfilingAnimalsBlotting, WesternCollagenEnergy MetabolismGene Expression RegulationGene Knockdown TechniquesMiceMitochondrial ProteinsMuscle, SkeletalMyostatinOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionCollagenMitochondrial ProteinsMyostatin

Identifiers

PMID19509079
PMCPMC3774565
OpenAlexW2149795455

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.