Evidence map›Paper›PMID 15470139›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Switching mature retinal ganglion cells to a robust growth state in vivo: gene expression and synergy with RhoA inactivation.

Dietmar Fischer, Victoria Petkova, Solon Thanos, Larry I Benowitz

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

111 citing papers in PubMed, 275 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Neural regeneration research · 2023
    Article
  8. Article
  9. Article
  10. Unleashing Intrinsic Growth Pathways in Regenerating Peripheral Neurons.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. The basic science of optic nerve regeneration.Annals of translational medicine · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. CXCR4/CXCL12-mediated entrapment of axons at the injury site compromises optic nerve regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Review
  20. Article

51 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Dietmar FischerLaboratories for Neuroscience Research in Neurosurgery, Children's Hospital, Boston, Massachusetts 02115, USA.
Victoria Petkova
Solon Thanos
Larry I Benowitz
Boston Children's Hospital · USBeth Israel Deaconess Hospital · USUniversity of Münster · DE

Funding

MOLECULAR BASES OF NEURONAL CONNECTIVITYR01EY005690 · NEI · MC LEAN HOSPITAL (BELMONT, MA) · PI BENOWITZ, LARRY IRA · 1985 to 2012
$4.7M
NEI NIH HHS EY05690NEI NIH HHS R01 EY005690
6 · The paper itself

Abstract

The inability of mature CNS neurons to regenerate injured axons has been attributed to a loss of inherent growth potential of cells and to inhibitory signals associated with myelin and the glial scar. The present study investigated two complementary issues: (1) whether mature CNS neurons can be stimulated to alter their gene expression profile and switch into a strong growth state; and (2) whether inactivating RhoA, a convergence point for multiple inhibitory signals, is sufficient to produce strong regeneration even without activating the growth state of neurons. In the mature rat, retinal ganglion cells (RGCs) normally fail to regenerate axons through the injured optic nerve but can be stimulated to do so by activating macrophages in the eye (e.g., by lens injury). To investigate underlying changes in gene expression, we retrogradely labeled RGCs with a fluorescent dye, performed optic nerve surgery with or without lens injury, and 4 d later, dissociated retinas, isolated RGCs by fluorescence-activated cell sorting, and examined their profiles of gene expression using microarrays. To investigate the effects of inactivating RhoA, we transfected RGCs with adeno-associated viruses carrying a gene for C3 ribosyltransferase. Our results show that, with appropriate stimulation, mature CNS neurons can undergo dramatic changes in gene expression comparable with those seen in regenerating neurons of the PNS, and that RhoA inactivation by itself results in moderate regeneration, and strongly potentiates axon regeneration through the mature optic nerve when the growth state of neurons is activated.

Indexed as

Gene ExpressionNerve RegenerationADP Ribose TransferasesAnimalsAxotomyBotulinum ToxinsCell Growth ProcessesCells, CulturedDependovirusFemaleGene Expression ProfilingGenetic VectorsImmunohistochemistryLens, CrystallineMacrophage ActivationOligonucleotide Array Sequence AnalysisADP Ribose TransferasesBotulinum Toxinsexoenzyme C3, Clostridium botulinumrhoA GTP-Binding Protein

Identifiers

PMID15470139
PMCPMC6729954
OpenAlexW2133782231

What Socratic 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 Socratic graph.