Evidence map›Paper›PMID 25257170›Full record

ArticleCell death and differentiation2015

Cell type-specific Nogo-A gene ablation promotes axonal regeneration in the injured adult optic nerve.

F Vajda, N Jordi, D Dalkara, S Joly, F Christ, B Tews, M E Schwab, V Pernet

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

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-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

24 citing papers in PubMed, 45 citations in OpenAlex.

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  9. Effects of Nogo-A and its receptor on the repair of sciatic nerve injury in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
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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

8 authors at 3 institutions in 2 countries.

F VajdaBrain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland.
N JordiBrain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland.
D Dalkara1] INSERM, U968, Paris, France [2] Sorbonne Universités, UPMC Univ Paris 06, UMR_S 968, Institut de la Vision, Paris, France [3] CNRS, UMR_7210, Paris F-75012, France.
S JolyBrain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland.
F ChristBrain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland.
B Tews1] Brain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland [2] German Cancer Research Center (DKFZ), Heidelberg University, Heidelberg, Germany.
M E SchwabBrain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland.
V PernetBrain Research Institute, University of Zurich, and Department of Health Sciences and Technology, ETH Zurich, CH-8057 Zurich, Switzerland.
University of Zurich · CHETH Zurich · CHInserm · FR

Funding

European Research Council 294115
6 · The paper itself

Abstract

Nogo-A is a well-known myelin-enriched inhibitory protein for axonal growth and regeneration in the central nervous system (CNS). Besides oligodendrocytes, our previous data revealed that Nogo-A is also expressed in subpopulations of neurons including retinal ganglion cells, in which it can have a positive role in the neuronal growth response after injury, through an unclear mechanism. In the present study, we analyzed the opposite roles of glial versus neuronal Nogo-A in the injured visual system. To this aim, we created oligodendrocyte (Cnp-Cre(+/-)xRtn4/Nogo-A(flox/flox)) and neuron-specific (Thy1-Cre(tg+)xRtn4(flox/flox)) conditional Nogo-A knock-out (KO) mouse lines. Following complete intraorbital optic nerve crush, both spontaneous and inflammation-mediated axonal outgrowth was increased in the optic nerves of the glia-specific Nogo-A KO mice. In contrast, neuron-specific deletion of Nogo-A in a KO mouse line or after acute gene recombination in retinal ganglion cells mediated by adeno-associated virus serotype 2.Cre virus injection in Rtn4(flox/flox) animals decreased axon sprouting in the injured optic nerve. These results therefore show that selective ablation of Nogo-A in oligodendrocytes and myelin in the optic nerve is more effective at enhancing regrowth of injured axons than what has previously been observed in conventional, complete Nogo-A KO mice. Our data also suggest that neuronal Nogo-A in retinal ganglion cells could participate in enhancing axonal sprouting, possibly by cis-interaction with Nogo receptors at the cell membrane that may counteract trans-Nogo-A signaling. We propose that inactivating Nogo-A in glia while preserving neuronal Nogo-A expression may be a successful strategy to promote axonal regeneration in the CNS.

Indexed as

RegenerationSignal TransductionAnimalsAxonsDependovirusFemaleGenetic VectorsMaleMiceMice, Inbred C57BLMice, KnockoutMyelin ProteinsMyelin SheathNerve CrushNeurogliaNeuronsMyelin ProteinsNogo ProteinsRtn4 protein, mouse

Identifiers

PMID25257170
PMCPMC4291493
OpenAlexW1968193820

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.