Evidence map›Paper›PMID 22648949›Full record

ArticleAmerican journal of physiology. Cell physiology2012

NOX2-dependent ROS is required for HDAC5 nuclear efflux and contributes to HDAC4 nuclear efflux during intense repetitive activity of fast skeletal muscle fibers.

Yewei Liu, Erick O Hernández-Ochoa, William R Randall, Martin F Schneider

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  4. Article
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Regulation of NADPH oxidases in skeletal muscle.Free radical biology & medicine · 2016
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Reactive oxygen species generation is not different during isometric and lengthening contractions of mouse muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  18. Article
  19. Review
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.

Yewei LiuDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201-1503, USA.
Erick O Hernández-Ochoa
William R Randall
Martin F Schneider
University of Maryland, Baltimore · US

Funding

Control of Calcium Release in Skeletal Muscle FibersR01AR055099 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI SCHNEIDER, MARTIN F · 2007 to 2011
$1.7M
Activity Dependent Signaling in Adult Skeletal Muscle Fiber PlasticityR01AR056477 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI SCHNEIDER, MARTIN F · 2008 to 2012
$1.6M
NIAMS NIH HHS R01 AR055099NIAMS NIH HHS R01 AR056477NIAMS NIH HHS R01-AR056477
6 · The paper itself

Abstract

Reactive oxygen species (ROS) have been linked to oxidation and nuclear efflux of class IIa histone deacetylase 4 (HDAC4) in cardiac muscle. Here we use HDAC-GFP fusion proteins expressed in isolated adult mouse flexor digitorum brevis muscle fibers to study ROS mediation of HDAC localization in skeletal muscle. H(2)O(2) causes nuclear efflux of HDAC4-GFP or HDAC5-GFP, which is blocked by the ROS scavenger N-acetyl-l-cysteine (NAC). Repetitive stimulation with 100-ms trains at 50 Hz, 2/s ("50-Hz trains") increased ROS production and caused HDAC4-GFP or HDAC5-GFP nuclear efflux. During 50-Hz trains, HDAC5-GFP nuclear efflux was completely blocked by NAC, but HDAC4-GFP nuclear efflux was only partially blocked by NAC and partially blocked by the calcium-dependent protein kinase (CaMK) inhibitor KN-62. Thus, during intense activity both ROS and CaMK play roles in nuclear efflux of HDAC4, but only ROS mediates HDAC5 nuclear efflux. The 10-Hz continuous stimulation did not increase the rate of ROS production and did not cause HDAC5-GFP nuclear efflux but promoted HDAC4-GFP nuclear efflux that was sensitive to KN-62 but not NAC and thus mediated by CaMK but not by ROS. Fibers from NOX2 knockout mice lacked ROS production and ROS-dependent nuclear efflux of HDAC5-GFP or HDAC4-GFP during 50-Hz trains but had unmodified Ca(2+) transients. Our results demonstrate that ROS generated by NOX2 could play important roles in muscle remodeling due to intense muscle activity and that the nuclear effluxes of HDAC4 and HDAC5 are differentially regulated by Ca(2+) and ROS during muscle activity.

Indexed as

1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAcetylcysteineAnimalsCalcium-Calmodulin-Dependent Protein KinasesEnzyme InhibitorsFemaleFree Radical ScavengersHistone DeacetylasesHydrogen PeroxideMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMuscle Fibers, Fast-TwitchNADPH Oxidase 2NADPH Oxidases1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAcetylcysteineCalcium-Calmodulin-Dependent Protein KinasesCybb protein, mouseEnzyme InhibitorsFree Radical ScavengersHdac5 protein, mouseHistone DeacetylasesHydrogen PeroxideKN 62Membrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesProtein KinasesReactive Oxygen SpeciesRecombinant Fusion Proteins

Identifiers

PMID22648949
PMCPMC3423023
OpenAlexW2105138628

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.