Evidence map›Paper›PMID 31133806›Full record

ArticleFrontiers in cellular neuroscience2019

From Ganglion Cell to Photoreceptor Layer: Timeline of Deterioration in a Rat Ischemia/Reperfusion Model.

Marina Palmhof, Viktoria Frank, Pascal Rappard, Emely Kortenhorn, Julia Demuth, Nora Biert, Gesa Stute, H Burkhard Dick, Stephanie C Joachim

Abstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Glaucoma Animal Models beyond Chronic IOP Increase.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. 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

9 authors.

Marina PalmhofExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Viktoria FrankExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Pascal RappardExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Emely KortenhornExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Julia DemuthExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Nora BiertExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Gesa StuteExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
H Burkhard DickExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.
Stephanie C JoachimExperimental Eye Research, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal damage and impaired vision in different retinal disorders are induced, among other factors, by ischemia/reperfusion (I/R). Since the mechanisms and the progression of ischemic injury are still not completely clarified, a timeline of this retinal degeneration is needed. In this study, we investigated protein and mRNA alterations at 2, 6, 12, and 24 h as well as 3 and 7 days after ischemia to determine the course of an ischemic insult through the whole retina. Moreover, functional analyses were performed at later stages. We detected a significant functional loss of cells in the inner nuclear layer and photoreceptors at 3 and 7 days. Additionally, the thickness of the whole retina was decreased at these points in time, indicating a severe degradation of all retinal layers. Immunohistological and qRT-PCR analyses of retinal ganglion cells (RGCs), glial cells, AII amacrine, cone and rod bipolar as well as cone and rod photoreceptor cells confirmed this first assumption. Our results show that all investigated cell types were damaged by ischemia induction. Especially RGCs, cone bipolar cells, and photoreceptor cones are very sensitive to I/R. These cells were lost shortly after ischemia induction with a progressive course up to 7 days. In addition, Müller cell gliosis was observed over the entire period of time. These results provide evidence, that I/R induces damage of the whole retina at early stages and increases over time. In conclusion, our study could demonstrate the intense impact of an ischemic injury. The ischemic defect spreads across the whole retina right up to the outer layers in the long-term and thus seems to impair the visual perception already during the stimulus processing. In addition, our findings indicate that the cone pathway seems to be particularly affected by this damage.

Indexed as

amacrine cellbipolar cellERGischemia/reperfusionphotoreceptorretinal ganglion cellretinal thicknesstimeline

Identifiers

PMID31133806
PMCPMC6524469

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.