Evidence map›Paper›PMID 25264029›Full record

ArticleMolecular and cellular neurosciences2014

A novel protective role for the innate immunity Toll-Like Receptor 3 (TLR3) in the retina via Stat3.

Amit K Patel, Abigail S Hackam

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  12. Protective Effects ofOxidative medicine and cellular longevity · 2018
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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

2 authors at 1 institution in 1 country.

Amit K PatelBascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Abigail S HackamBascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA. Electronic address: ahackam@med.miami.edu.
University of Miami · US

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Victor L Perez · 2004 to 2026
$12.2M
WNT SIGNALING AND NEUROPROTECTION IN THE RETINAR01EY017837 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HACKAM, ABIGAIL S · 2007 to 2011
$2.0M
NEI NIH HHS P30 EY014801NEI NIH HHS P30EY014801NEI NIH HHS R01 EY017837
6 · The paper itself

Abstract

The innate immune system and inflammatory pathways play key roles in numerous diseases of the central nervous system (CNS). Recent evidence indicates that innate immunity induces both pathogenesis and protection during neuronal injury. To test the possibility that the conflicting roles of innate immunity in the CNS depends on the cellular environment in which innate immunity is stimulated, we analyzed the effect of Toll-Like Receptor 3 (TLR3) activation on neuronal survival in the presence and absence of oxidative injury in a mouse model system. We demonstrated that activation of TLR3 by the double stranded RNA activator, Poly (I:C), during paraquat induced oxidative stress, significantly protected mouse photoreceptors, as measured by increased retinal structure, function, and improved visual acuity. In contrast, TLR3 activation without concurrent oxidative injury was neurotoxic. The neurotoxic and protective effects of Poly (I:C) stimulation were absent in TLR3 knockout animals, which indicates that protection by Poly (I:C) is dependent on the TLR3 signaling pathway. Furthermore, we identified the pro-survival transcription factor Stat3 as a necessary mechanism for protection. Knockdown of Stat3 using lentivirally delivered shRNA abolished the protective effects of TLR3 signaling in the retina during oxidative stress. Therefore, TLR3 activation in the context of oxidative stress triggers protective instead of pathogenic signaling, suggesting that TLR3 is a potential therapeutic target for neurodegeneration where oxidative stress is a significant contributor.

Indexed as

AnimalsCell SurvivalFemaleMaleMiceOxidative StressRetinaSTAT3 Transcription FactorToll-Like Receptor 3STAT3 Transcription FactorTLR3 protein, mouseToll-Like Receptor 3Age-related macular degeneration (AMD)Innate immunityNeuroprotectionOxidative stressPhotoreceptorsRetinal degenerationStat3Toll-Like Receptor 3 (TLR3)

Identifiers

PMID25264029
PMCPMC4250317
OpenAlexW1970769682

What OpenQuestion 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 OpenQuestion graph.