Evidence map›Paper›PMID 24077965›Full record

ArticleDisease models & mechanisms2014

Molecular mechanism of sphingosine-1-phosphate action in Duchenne muscular dystrophy.

Diem-Hang Nguyen-Tran, Nitai C Hait, Henrik Sperber, Junlin Qi, Karin Fischer, Nick Ieronimakis, Mario Pantoja, Aislinn Hays, Jeremy Allegood, Morayma Reyes and 2 more

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Current Pharmacological Strategies for Duchenne Muscular Dystrophy.Frontiers in cell and developmental biology · 2021
    Review
  9. Review
  10. Regulation of hypoxia-inducible factor functions in the nucleus by sphingosine-1-phosphate.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  11. Review
  12. S1P/S1P Receptor Signaling in Neuromuscolar Disorders.International journal of molecular sciences · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Epigenetics and Sphingolipid Metabolism in Health and Disease.International journal of biopharmaceutical sciences · 2018
    Article
  19. 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

12 authors at 2 institutions in 1 country.

Diem-Hang Nguyen-TranMolecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195-7350, USA.
Nitai C Hait
Henrik Sperber
Junlin Qi
Karin Fischer
Nick Ieronimakis
Mario Pantoja
Aislinn Hays
Jeremy Allegood
Morayma Reyes
Sarah Spiegel
Hannele Ruohola-Baker
University of Washington · USVirginia Commonwealth University · US

Funding

SPECIFICITY OF OXYGEN DNA DAMAGE AND MUTAGENESISP01AG001751 · NIA · UNIVERSITY OF WASHINGTON · PI PRUSKY, GLEN THOMAS · 1985 to 2021
$29.6M
Self Renewal and Differentiation of Human Embryonic Stem CellsP01GM081619 · NIGMS · UNIVERSITY OF WASHINGTON · PI WARE, CAROL B · 2007 to 2017
$20.6M
GENETIC APPROACHES TO AGING RESEARCHT32AG000057 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 1985 to 2019
$14.2M
SPHINGOSINE AS A MODULATOR OF CELLULAR PROLIFERATIONR01GM043880 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 1990 to 2023
$3.8M
Sphingosine Kinases in Cancer Cell SignalingR01CA061774 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 1994 to 2015
$3.8M
Sphingosine-1 phosphate phosphohydrolaseR37GM043880 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 2003 to 2012
$3.2M
MicroRNA Function in Human Embryonic Stem CellsR01GM083867 · NIGMS · UNIVERSITY OF WASHINGTON · PI RUOHOLA-BAKER, HANNELE · 2008 to 2011
$1.5M
Acquisition of Embryonic Stem Cell Metabolic Signature - Minority SupplementR01GM097372 · NIGMS · UNIVERSITY OF WASHINGTON · PI RUOHOLA-BAKER, HANNELE · 2011 to 2014
$1.3M
Generation of Wunen/LPP3-based therapy for muscular dystrophyRC1AR058520 · NIAMS · UNIVERSITY OF WASHINGTON · PI RUOHOLA-BAKER, HANNELE · 2009 to 2010
$928k
NCI NIH HHS R01 CA061774NIAMS NIH HHS 5RC1AR058520NIAMS NIH HHS RC1 AR058520NIA NIH HHS P01 AG001751NIA NIH HHS T32 AG000057NIA NIH HHS T32 AG00057NIGMS NIH HHS 1P01GM081619NIGMS NIH HHS P01 GM081619NIGMS NIH HHS R01 GM043880NIGMS NIH HHS R01 GM083867NIGMS NIH HHS R01GM083867NIGMS NIH HHS R01 GM097372NIGMS NIH HHS R01GM097372NIGMS NIH HHS R37 GM043880NIGMS NIH HHS R37GM043880
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a lethal muscle-wasting disease. Studies in Drosophila showed that genetic increase of the levels of the bioactive sphingolipid sphingosine-1-phosphate (S1P) or delivery of 2-acetyl-5-tetrahydroxybutyl imidazole (THI), an S1P lyase inhibitor, suppresses dystrophic muscle degeneration. In the dystrophic mouse (mdx), upregulation of S1P by THI increases regeneration and muscle force. S1P can act as a ligand for S1P receptors and as a histone deacetylase (HDAC) inhibitor. Because Drosophila has no identified S1P receptors and DMD correlates with increased HDAC2 levels, we tested whether S1P action in muscle involves HDAC inhibition. Here we show that beneficial effects of THI treatment in mdx mice correlate with significantly increased nuclear S1P, decreased HDAC activity and increased acetylation of specific histone residues. Importantly, the HDAC2 target microRNA genes miR-29 and miR-1 are significantly upregulated, correlating with the downregulation of the miR-29 target Col1a1 in the diaphragm of THI-treated mdx mice. Further gene expression analysis revealed a significant THI-dependent decrease in inflammatory genes and increase in metabolic genes. Accordingly, S1P levels and functional mitochondrial activity are increased after THI treatment of differentiating C2C12 cells. S1P increases the capacity of the muscle cell to use fatty acids as an energy source, suggesting that THI treatment could be beneficial for the maintenance of energy metabolism in mdx muscles.

Indexed as

AcetylationAldehyde-LyasesAnimalsCell NucleusDown-RegulationHistone DeacetylasesHistonesImidazolesInflammationLysophospholipidsMaleMiceMice, Inbred C57BLMice, Inbred mdxMicroRNAsMitochondria2-acetyl-4(5)-tetrahydroxybutylimidazoleAldehyde-LyasesHistone DeacetylasesHistonesImidazolesLysophospholipidsMicroRNAsMirn1 microRNA, mouseMIRN29 microRNA, mouseProtein KinasesSphingosinesphingosine 1-phosphatesphingosine 1-phosphate lyase (aldolase)titin protein, mousedysDystrophinHDACmdxS1PTHI

Identifiers

PMID24077965
PMCPMC3882047
OpenAlexW2113340784

What OpenQuestion holds

Textmetadata
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.