Evidence map›Paper›PMID 32396062›Full record

ArticleeLife2020

Tgfb3 collaborates with PP2A and notch signaling pathways to inhibit retina regeneration.

Mi-Sun Lee, Jin Wan, Daniel Goldman

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. 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
2.6field-weighted citation impact, top 9% 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, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. eLife · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Advances in the study of Müller glia reprogramming in mammals.Frontiers in cellular neuroscience · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Retinal regeneration requires dynamic Notch signaling.Neural regeneration research · 2022
    Review
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 1 institution in 1 country.

Mi-Sun Lee *Michigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, United States.
Jin Wan *Michigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, United States.
Daniel GoldmanMichigan Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, United States.ORCID 0000-0002-0013-1188
University of Michigan · US

Funding

Muller glia and retina regeneration-Diversity supplementR01EY018132 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOLDMAN, DANIEL J · 2007 to 2019
$4.8M
Muller glia heterogeneity and progenitor fateR01EY027310 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GOLDMAN, DANIEL J · 2017 to 2020
$1.2M
Gilbert Family Foundation AWD011459Gilbert Family Foundation, Vision Restoration Initiative AWD011459NEI NIH HHS R01 EY018132NEI NIH HHS R01 EY027310
6 · The paper itself

Abstract

Neuronal degeneration in the zebrafish retina stimulates Müller glia (MG) to proliferate and generate multipotent progenitors for retinal repair. Controlling this proliferation is critical to successful regeneration. Previous studies reported that retinal injury stimulates pSmad3 signaling in injury-responsive MG. Contrary to these findings, we report pSmad3 expression is restricted to quiescent MG and suppressed in injury-responsive MG. Our data indicates that Tgfb3 is the ligand responsible for regulating pSmad3 expression. Remarkably, although overexpression of either Tgfb1b or Tgfb3 can stimulate pSmad3 expression in the injured retina, only Tgfb3 inhibits injury-dependent MG proliferation; suggesting the involvement of a non-canonical Tgfb signaling pathway. Furthermore, inhibition of Alk5, PP2A or Notch signaling rescues MG proliferation in Tgfb3 overexpressing zebrafish. Finally, we report that this Tgfb3 signaling pathway is active in zebrafish MG, but not those in mice, which may contribute to the different regenerative capabilities of MG from fish and mammals.

Indexed as

Nerve RegenerationAnimalsCell ProliferationCellular ReprogrammingFemaleGene Expression RegulationMaleNeurogliaProtein Phosphatase 2Receptors, NotchReceptor, Transforming Growth Factor-beta Type IRetinaSignal TransductionSmad3 ProteinTransforming Growth Factor beta3ZebrafishProtein Phosphatase 2Receptors, NotchReceptor, Transforming Growth Factor-beta Type ISmad3 ProteinTransforming Growth Factor beta3Zebrafish Proteinsmuller glianotchPP2Aregenerative medicineSmadstem cellstem cellsTgfbzebrafish

Identifiers

PMID32396062
PMCPMC7250569
OpenAlexW3025614476

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.