Evidence map›Paper›PMID 25595590›Full record

ArticleJournal of neuroinflammation2015

Chemokine-mediated inflammation in the degenerating retina is coordinated by Müller cells, activated microglia, and retinal pigment epithelium.

Matt Rutar, Riccardo Natoli, R X Chia, Krisztina Valter, Jan M Provis

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 128 citations in OpenAlex.

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

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 1 institution in 1 country.

Matt RutarJohn Curtin School of Medical Research, The Australian National University, Building 131, Garran Road, Canberra, ACT 2601, Australia. matt.rutar@anu.edu.au.
Riccardo NatoliJohn Curtin School of Medical Research, The Australian National University, Building 131, Garran Road, Canberra, ACT 2601, Australia. riccardo.natoli@anu.edu.au.
R X ChiaJohn Curtin School of Medical Research, The Australian National University, Building 131, Garran Road, Canberra, ACT 2601, Australia. u4957724@anu.edu.au.
Krisztina ValterJohn Curtin School of Medical Research, The Australian National University, Building 131, Garran Road, Canberra, ACT 2601, Australia. jan.provis@anu.edu.au.
Jan M ProvisJohn Curtin School of Medical Research, The Australian National University, Building 131, Garran Road, Canberra, ACT 2601, Australia. krisztina.valter-kocsi@anu.edu.au.
Australian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMonocyte infiltration is involved in the pathogenesis of many retinal degenerative conditions. This process traditionally depends on local expression of chemokines, though the roles of many of these in the degenerating retina are unclear. Here, we investigate expression and in situ localization of the broad chemokine response in a light-induced model of retinal degeneration.

methodsSprague-Dawley (SD) rats were exposed to 1,000 lux light damage (LD) for up to 24 hrs. At time points during (1 to 24 hrs) and following (3 and 7 days) exposure, animals were euthanized and retinas processed. Microarray analysis assessed differential expression of chemokines. Some genes were further investigated using polymerase chain reaction (PCR) and in situ hybridization and contrasted with photoreceptor apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Recruitment of retinal CD45 (+) leukocytes was determined via fluorescence activated cell sorting (FACS), and expression of chemokine receptors determined using PCR.

resultsExposure to 24 hrs of LD resulted in differential expression of chemokines including Ccl3, Ccl4, Ccl7, Cxcl1, and Cxcl10. Their upregulation correlated strongly with peak photoreceptor death, at 24 hrs exposure. In situ hybridization revealed that the modulated chemokines were expressed by a combination of Müller cells, activated microglia, and retinal pigment epithelium (RPE). This preceded large increases in the number of CD45(+) cells at 3- and 7-days post exposure, which expressed a corresponding repertoire of chemokine receptors.

conclusionsOur data indicate that retinal degeneration induces upregulation of a broad chemokine response whose expression is coordinated by Müller cells, microglia, and RPE. The findings inform our understanding of the processes govern the trafficking of leukocytes, which are contributors in the pathology of retinal degenerations.

Indexed as

AnimalsCell DeathChemokinesDisease Models, AnimalEpendymoglial CellsFlow CytometryGene Expression RegulationInflammationLightMicroarray AnalysisMicrogliaPhotoreceptor CellsRatsRats, Sprague-DawleyRetinaRetinal DegenerationChemokinesRNA, Messenger

Identifiers

PMID25595590
PMCPMC4308937
OpenAlexW2000919900

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.