Evidence map›Paper›PMID 24747725›Full record

ArticlePloS one2014

Proliferation potential of Müller glia after retinal damage varies between mouse strains.

Akiko Suga, Kazuyo Sadamoto, Momo Fujii, Michiko Mandai, Masayo Takahashi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact, top 98% 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

29 citing papers in PubMed, 0 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Cell-Based Therapies: Strategies for Regeneration.Cold Spring Harbor perspectives in medicine · 2023
    Review
  7. Nestin Regulates Müller Glia Proliferation After Retinal Injury.Investigative ophthalmology & visual science · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. ARL13B, a Joubert Syndrome-Associated Protein, Is Critical for Retinogenesis and Elaboration of Mouse Photoreceptor Outer Segments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 3 institutions in 1 country.

Akiko SugaLaboratory for Retinal Regeneration, Center for Developmental Biology, RIKEN, Minatojima, Chu-O-ku, Kobe, Japan.
Kazuyo SadamotoLaboratory for Retinal Regeneration, Center for Developmental Biology, RIKEN, Minatojima, Chu-O-ku, Kobe, Japan.
Momo FujiiLaboratory for Retinal Regeneration, Center for Developmental Biology, RIKEN, Minatojima, Chu-O-ku, Kobe, Japan.
Michiko MandaiLaboratory for Retinal Regeneration, Center for Developmental Biology, RIKEN, Minatojima, Chu-O-ku, Kobe, Japan.
Masayo TakahashiLaboratory for Retinal Regeneration, Center for Developmental Biology, RIKEN, Minatojima, Chu-O-ku, Kobe, Japan.
Development Bank of Japan · JPRIKEN Center for Biosystems Dynamics Research · JPTokyo Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinal Müller glia can serve as a source for regeneration of damaged retinal neurons in fish, birds and mammals. However, the proliferation rate of Müller glia has been reported to be low in the mammalian retina. To overcome this problem, growth factors and morphogens have been studied as potent promoters of Müller glial proliferation, but the molecular mechanisms that limit the proliferation of Müller glia in the mammalian retina remain unknown. In the present study, we found that the degree of damage-induced Müller glia proliferation varies across mouse strains. In mouse line 129×1/SvJ (129), there was a significantly larger proliferative response compared with that observed in C57BL/6 (B6) after photoreceptor cell death. Treatment with a Glycogen synthase kinase 3 (GSK3) inhibitor enhanced the proliferation of Müller glia in 129 but not in B6 mouse retinas. We therefore focused on the different gene expression patterns during retinal degeneration between B6 and 129. Expression levels of Cyclin D1 and Nestin correlated with the degree of Müller glial proliferation. A comparison of genome-wide gene expression between B6 and 129 showed that distinct sets of genes were upregulated in the retinas after damage, including immune response genes and chromatin remodeling factors.

Indexed as

AnimalsBiomarkersCell CycleCell ProliferationChromatin Assembly and DisassemblyEpendymoglial CellsGlycogen Synthase Kinase 3MaleMiceProtein Kinase InhibitorsRetinaSpecies SpecificityTranscriptomeBiomarkersGlycogen Synthase Kinase 3Protein Kinase Inhibitors

Identifiers

PMID24747725
PMCPMC3991641
OpenAlexW910166807

What OpenQuestion holds

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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.