Evidence map›Paper›PMID 19733561›Full record

ArticleExperimental neurology2010

Rolipram-induced elevation of cAMP or chondroitinase ABC breakdown of inhibitory proteoglycans in the extracellular matrix promotes peripheral nerve regeneration.

E Udina, A Ladak, M Furey, T Brushart, N Tyreman, T Gordon

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

22 citing papers in PubMed, 61 citations in OpenAlex.

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  9. MBD1 Contributes to the Genesis of Acute Pain and Neuropathic Pain by Epigenetic Silencing ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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  16. Electrical Stimulation to Enhance Axon Regeneration After Peripheral Nerve Injuries in Animal Models and Humans.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  17. Review
  18. Article
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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

6 authors at 1 institution in 2 countries.

E UdinaDivision of Physical Medicine and Rehabilitation, Faculty of Medicine and Dentistry, Center for Neurosciences, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
A Ladak
M Furey
T Brushart
N Tyreman
T Gordon
University of Alberta · CA

Funding

MOTOR/SENSORY SPECIFICITY--MECHANISMS AND AUGMENTATIONR01NS034484 · NINDS · JOHNS HOPKINS UNIVERSITY · PI BRUSHART, THOMAS M · 1997 to 2013
$4.5M
CIHRNINDS NIH HHS R01 NS034484
6 · The paper itself

Abstract

The inhibitory growth environment of myelin and extracellular matrix proteoglycans in the central nervous system may be overcome by elevating neuronal cAMP or degrading inhibitory proteoglycans with chondroitinase ABC (ChABC). In this study, we asked whether similar mechanisms operate in peripheral nerve regeneration where effective Wallerian degeneration removes myelin and extracellular proteoglycans slowly. We repaired transected common peroneal (CP) nerve in rats and either elevated cAMP in the axotomized neurons by subcutaneous rolipram, a specific inhibitor of phosphodiesterase IV, and/or promoted degradation of proteoglycans in the distal nerve stump by local ChABC administration. Rolipram treatment significantly increased the number of motoneurons that regenerated axons across the repair site at 1 and 2 weeks, and increased the number of sensory neurons that regenerated axons across the repair site at 2 weeks. Local application of ChABC had a similar effect to rolipram treatment in promoting motor axon regeneration, the effect being no greater when rolipram and ChABC were administered simultaneously. We conclude that blocking inhibitors of axon regeneration by elevating cAMP or degrading proteoglycans in the distal nerve stump promotes peripheral axon regeneration after surgical repair of a transected nerve. It is likely that elevated cAMP is sufficient to encourage axon outgrowth despite the inhibitory growth environment such that simultaneous enzymatic proteoglycan degradation does not promote more axon regeneration than either elevated cAMP or proteoglycan degradation alone.

Indexed as

Analysis of VarianceAnimalsChondroitin ABC LyaseCyclic AMPDisease Models, AnimalExtracellular MatrixFemaleGanglia, SpinalInjections, SubcutaneousMicroscopy, Electron, TransmissionMotor NeuronsNerve RegenerationPeroneal NeuropathiesPhosphodiesterase InhibitorsProteoglycansRatsChondroitin ABC LyaseCyclic AMPPhosphodiesterase InhibitorsProteoglycansRolipram

Identifiers

PMID19733561
PMCPMC3071985
OpenAlexW2023132002

What OpenQuestion holds

Textmetadata
LicenceTDM
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.