Evidence map›Paper›PMID 15872101›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

The genomic response to retinal disease and injury: evidence for endothelin signaling from photoreceptors to glia.

Amir Rattner, Jeremy Nathans

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

114 citing papers in PubMed, 213 citations in OpenAlex.

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  9. RAAS in diabetic retinopathy: mechanisms and therapies.Archives of endocrinology and metabolism · 2024
    Review
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  12. Role of Serine Protease Inhibitors A1 and A3 in Ocular Pathologies.Investigative ophthalmology & visual science · 2024
    Review
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  16. Genetic spectrum, retinal phenotype, and peripapillary RNFL thickness in RPGR heterozygotes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
    Article
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54 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

2 authors at 2 institutions in 1 country.

Amir RattnerDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. arattner@jhmi.edu
Jeremy Nathans
Howard Hughes Medical Institute · USJohns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regardless of proximal cause, photoreceptor injury or disease almost invariably leads to the activation of Muller cells, the principal glial cells in the retina. This observation implies the existence of signaling systems that inform Muller cells of the health status of photoreceptors. It further suggests that diverse types of photoreceptor damage elicit a limited range of biochemical responses. Using the mouse retina, we show by microarray, RNA blot, and in situ hybridization that the genomic responses to both light damage and inherited photoreceptor degeneration involve a relatively small number of genes and that the genes activated by these two insults overlap substantially with one another and with the genes activated by retinal detachment. Among the induced transcripts, those coding for endothelin2 (Edn2) are unusual in that they are localized to photoreceptors and are also highly induced in all of the tested models of photoreceptor disease or injury. Acute light damage also leads to a >10-fold increase in endothelin receptor B (Ednrb) in Muller cells 24 h after injury. These observations suggest that photoreceptor-derived EDN2 functions as a general stress signal, that EDN2 signals to Muller cells by binding to EDNRB, and that Muller cells can increase their sensitivity to EDN2 as part of the injury response.

Indexed as

GenomicsAnimalsAnnexin A2Aspartate CarbamoyltransferaseBlotting, NorthernBlotting, WesternCarbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)CeruloplasminDihydroorotaseDisease Models, AnimalEndothelin-2Endothelin Receptor AntagonistsEndothelinsFluorescent Antibody TechniqueGene Expression RegulationGlial Fibrillary Acidic ProteinAnnexin A2Aspartate CarbamoyltransferaseCAD trifunctional enzymeCarbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)Ceruloplasmincyclo(Trp-Asp-Pro-Val-Leu)DihydroorotaseEndothelin-2Endothelin Receptor AntagonistsEndothelinsGlial Fibrillary Acidic ProteinIntermediate Filament ProteinsMembrane GlycoproteinsNerve Tissue ProteinsPeptides, CyclicPeripherinsReceptors, Endothelin

Identifiers

PMID15872101
PMCPMC6725023
OpenAlexW2074832091

What OpenQuestion 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 OpenQuestion graph.