Evidence map›Paper›PMID 9614240›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Inhibition of CPP32-like proteases rescues axotomized retinal ganglion cells from secondary cell death in vivo.

P Kermer, N Klöcker, M Labes, M Bähr

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 194 citations in OpenAlex.

  1. Review
  2. Ouabain-NaNeurochemical research · 2022
    Article
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  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Role of Protease-Inhibitors in Ocular Diseases.Molecules (Basel, Switzerland) · 2014
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Involvement of caspase-6 and caspase-8 in neuronal apoptosis and the regenerative failure of injured retinal ganglion cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  19. 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

4 authors at 1 institution in 1 country.

P KermerDepartment of Neurology, Universität Tübingen, 72076 Tübingen, Germany.
N Klöcker
M Labes
M Bähr
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The majority of retinal ganglion cells (RGCs) degenerate and die after transection of the optic nerve (ON) in the adult rat. This secondary cell death can primarily be ascribed to apoptosis. Recent work strongly suggests a decisive role for a family of cysteine proteases, termed caspases, as mediators of neuronal apoptosis. In this study, we investigated whether activation of caspases contributes to delayed death of RGCs after axotomy. Intraocular application of various caspase inhibitors rescued up to 34% of RGCs that would otherwise have died 14 d after ON transection. Using a modified affinity-labeling technique, we detected a 17 kDa protease subunit upregulated after axotomy. Upregulation was prevented by caspase inhibitor treatment. The 17 kDa protein was identified as a CPP32-like protease by Western blot analysis and affinity labeling with biotinylated acetyl-Asp-Glu-Val-Asp-aldehyde, which specifically inhibits CPP32-like caspases. In vivo application of the irreversible caspase inhibitor benzyloxycarbonyl-Asp-Glu-Val-Asp-chloromethylketone revealed CPP32-like proteases to be major mediators of caspase-induced apoptosis in axotomized RGCs, because this inhibitor showed an even higher neuroprotective potential than the irreversible wide-range inhibitor benzyloxycarbonyl-Val-Ala-DL-Asp-fluoromethylketone. In summary, the data presented here provide further insight into the mechanisms of injury-induced neuronal apoptosis and could give rise to more effective therapeutic intervention strategies in CNS trauma and neurodegenerative diseases.

Indexed as

AxotomyCaspasesAmino Acid Chloromethyl KetonesAnimalsCaspase 3Cell DeathCysteine EndopeptidasesDenervationEndopeptidasesEnzyme ActivationFemaleOptic NerveRatsRats, Sprague-DawleyRetinal Ganglion CellsAmino Acid Chloromethyl Ketonesbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCasp3 protein, ratCaspase 3CaspasesCysteine EndopeptidasesEndopeptidases

Identifiers

PMID9614240
PMCPMC6792678
OpenAlexW1760718049

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.