Evidence map›Paper›PMID 20484625›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

MAG and OMgp synergize with Nogo-A to restrict axonal growth and neurological recovery after spinal cord trauma.

William B J Cafferty, Philip Duffy, Eric Huebner, Stephen M Strittmatter

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 1 synthesis or guideline pooled it, 252 citations in OpenAlex.

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87 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

William B J CaffertyProgram in Cellular Neuroscience, Neurodegeneration, and Repair, Yale University School of Medicine, New Haven, Connecticut 06536, USA.
Philip Duffy
Eric Huebner
Stephen M Strittmatter
Neurology, Inc · USYale University · US

Funding

MOLECULAR DETERMINANTS OF AXONAL REGENERATIONR01NS039962 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2000 to 2010
$3.9M
Nogo Receptor in Axonal RegenerationR01NS042304 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2001 to 2010
$3.3M
Axonal Growth Cone Signal TransductionR37NS033020 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2005 to 2011
$2.9M
Nogo Receptor Antagonist for Ischemic Stroke RecoveryR01NS056485 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2006 to 2010
$1.4M
NINDS NIH HHS R01 NS039962NINDS NIH HHS R01 NS042304NINDS NIH HHS R01 NS056485NINDS NIH HHS R37 NS033020
6 · The paper itself

Abstract

Functional recovery after adult CNS damage is limited in part by myelin inhibitors of axonal regrowth. Three molecules, Nogo-A, MAG, and OMgp, are produced by oligodendrocytes and share neuronal receptor mechanisms through NgR1 and PirB. While each has an axon-inhibitory role in vitro, their in vivo interactions and relative potencies have not been defined. Here, we compared mice singly, doubly, or triply mutant for these three myelin inhibitor proteins. The myelin extracted from Nogo-A mutant mice is less inhibitory for axons than is that from wild-type mice, but myelin lacking MAG and OMgp is indistinguishable from control. However, myelin lacking all three inhibitors is less inhibitory than Nogo-A-deficient myelin, uncovering a redundant and synergistic role for all three proteins in axonal growth inhibition. Spinal cord injury studies revealed an identical in vivo hierarchy of these three myelin proteins. Loss of Nogo-A allows corticospinal and raphespinal axon growth above and below the injury, as well as greater behavioral recovery than in wild-type or heterozygous mutant mice. In contrast, deletion of MAG and OMgp stimulates neither axonal growth nor enhanced locomotion. The triple-mutant mice exhibit greater axonal growth and improved locomotion, consistent with a principal role for Nogo-A and synergistic actions for MAG and OMgp, presumably through shared receptors. These data support the hypothesis that targeting all three myelin ligands, as with NgR1 decoy receptor, provides the optimal chance for overcoming myelin inhibition and improving neurological function.

Indexed as

Analysis of VarianceAnimalsBiotinCells, CulturedDextransDisease Models, AnimalFemaleFunctional LateralityGanglia, SpinalGPI-Linked ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMutationMyelin-Associated GlycoproteinBiotinbiotinylated dextran amineDextransGPI-Linked ProteinsMag protein, mouseMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsNerve Tissue ProteinsNogo ProteinsOmg protein, mouseReceptors, Cell SurfaceReceptors, SerotoninRtn4 protein, mouse

Identifiers

PMID20484625
PMCPMC2883258
OpenAlexW2021318239

What OpenQuestion holds

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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.