Evidence map›Paper›PMID 15968082›Full record

ArticleJournal of molecular neuroscience : MN2005

Axotomy-induced early down-regulation of POU-IV class transcription factors Brn-3a and Brn-3b in retinal ganglion cells.

Jochen H Weishaupt, Nikolaj Klöcker, Mathias Bähr

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2005. 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
0.6field-weighted citation impact, top 44% 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, 40 citations in OpenAlex.

  1. Article
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  4. Targeting HDAC3 Activity with RGFP966 Protects Against Retinal Ganglion Cell Nuclear Atrophy and Apoptosis After Optic Nerve Injury.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2018
    Article
  5. AAV2-Mediated Transduction of the Mouse Retina After Optic Nerve Injury.Investigative ophthalmology & visual science · 2017
    Article
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  12. DLK initiates a transcriptional program that couples apoptotic and regenerative responses to axonal injury.Proceedings of the National Academy of Sciences of the United States of America · 2013
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  18. Localization of a wide-ranging panel of antigens in the rat retina by immunohistochemistry: comparison of Davidson's solution and formalin as fixatives.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011
    Article
  19. Early microglia activation in a mouse model of chronic glaucoma.The Journal of comparative neurology · 2011
    Article
  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

3 authors at 2 institutions in 1 country.

Jochen H WeishauptDepartment of Neurology, University of Göttingen, Göttingen, Germany.
Nikolaj Klöcker
Mathias Bähr
University of Göttingen · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been proposed that neurons being exposed to proapoptotic stimuli undergo dedifferentiation, a process that can either allow for regeneration and axon regrowth or, if remaining incomplete, can force the cell to activate apoptotic pathways. A pivotal step in the differentiation program from neuronal precursor cells to differentiated, postmitotic neurons is their exit from the cell cycle. The POU domain transcription factors Brn-3b and Brn-3a, which are expressed in retinal ganglion cells (RGCs) directly after the exit of RGC precursors from the cell cycle, can be employed as RGC-specific differentiation markers to study potential dedifferentiation of RGCs after axotomy. Here, we examined mRNAand protein expression of Brn-3a and -3b in rat RGCs following axonal lesion. We observed a rapid down-regulation of Brn-3a and -3b protein expression in axotomized RGCs, clearly preceding apoptosis of RGCs. Using real-time PCR, we show that regulation of Brn-3 expression occurred at the transcriptional level. The small subset of RGCs regenerating into a peripheral nerve graft did not (re-)express Brn-3a or -b. In conclusion, we found further evidence supporting the hypothesis of a dedifferentiation process in severed mature neurons. As Brn-3b expression has been shown to be a prerequisite for developmental survival of most RGCs and Brn-3a activates transcription of anti-apoptotic genes, down-regulation of Brn-3 transcription factors might be causally involved in the secondary death of adult RGCs following axotomy.

Indexed as

AxotomyGene Expression RegulationAnimalsApoptosisCell NucleusDNA-Binding ProteinsMaleNerve RegenerationRatsRats, Sprague-DawleyRetinal Ganglion CellsReverse Transcriptase Polymerase Chain ReactionTranscription Factor Brn-3Transcription Factor Brn-3BTranscription FactorsTranscription, GeneticDNA-Binding ProteinsTranscription Factor Brn-3Transcription Factor Brn-3BTranscription Factors

Identifiers

PMID15968082
OpenAlexW1977155385

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.