Evidence map›Paper›PMID 27564592›Full record

ArticleThe European journal of neuroscience2016

Virally delivered, constitutively active NFκB improves survival of injured retinal ganglion cells.

Galina Dvoriantchikova, Steve Pappas, Xueting Luo, Marcio Ribeiro, Dagmara Danek, Daniel Pelaez, Kevin K Park, Dmitry Ivanov

Abstract read
In one paragraph

Article in The European journal of neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. CaeNeuro · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Strategies to Promote Long-Distance Optic Nerve Regeneration.Frontiers in cellular neuroscience · 2020
    Article
  11. Article
  12. 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

8 authors at 1 institution in 1 country.

Galina DvoriantchikovaDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Steve PappasDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Xueting LuoMiami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA.
Marcio RibeiroMiami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA.
Dagmara DanekDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Daniel PelaezDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Kevin K ParkMiami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA.
Dmitry IvanovDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
University of Miami · US

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Victor L Perez · 2004 to 2026
$12.2M
Regeneration and Reconnection of Damaged Optic NerveR01EY022961 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PARK, KEVIN KYUNG · 2013 to 2019
$2.1M
Role of toll-like receptor signaling in retinal ischemiaR01EY022348 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI IVANOV, DMITRY V · 2012 to 2014
$1.1M
NEI NIH HHS P30 EY014801NEI NIH HHS R01 EY022348NEI NIH HHS R01 EY022961
6 · The paper itself

Abstract

As axon damage and retinal ganglion cell (RGC) loss lead to blindness, therapies that increase RGC survival and axon regrowth have direct clinical relevance. Given that NFκB signaling is critical for neuronal survival and may regulate neurite growth, we investigated the therapeutic potential of NFκB signaling in RGC survival and axon regeneration. Although both NFκB subunits (p65 and p50) are present in RGCs, p65 exists in an inactive (unphosphorylated) state when RGCs are subjected to neurotoxic conditions. In this study, we used a phosphomimetic approach to generate DNA coding for an activated (phosphorylated) p65 (p65mut), then employed an adeno-associated virus serotype 2 (AAV2) to deliver the DNA into RGCs. We tested whether constitutive p65mut expression prevents death and facilitates neurite outgrowth in RGCs subjected to transient retinal ischemia or optic nerve crush (ONC), two models of neurotoxicity. Our data indicate that RGCs treated with AAV2-p65mut displayed a significant increase in survival compared to controls in ONC model (77 ± 7% vs. 25 ± 3%, P-value = 0.0001). We also found protective effect of modified p65 in RGCs of ischemic retinas (55 ± 12% vs. 35 ± 6%), but not to a statistically significant degree (P-value = 0.14). We did not detect a difference in axon regeneration between experimental and control animals after ONC. These findings suggest that increased NFκB signaling in RGCs attenuates retinal damage in animal models of neurodegeneration, but insignificantly impacts axon regeneration.

Indexed as

Nerve RegenerationAnimalsAxonsCell LineCells, CulturedDependovirusGenetic TherapyMiceMice, Inbred C57BLNeuronal OutgrowthOptic Nerve InjuriesRetinal Ganglion CellsTranscription Factor RelATranscription Factor RelAadeno-associated virus serotype 2optic nerve crush modelphosphomimeticretinal ganglion cellstransient retinal ischemia model

Identifiers

PMID27564592
PMCPMC5138106
OpenAlexW2508157715

What Socratic holds

Textmetadata
LicenceTDM
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.