Evidence map›Paper›PMID 27107718›Full record

ArticleJournal of neuroinflammation2016

Aquaporin 11, a regulator of water efflux at retinal Müller glial cell surface decreases concomitant with immune-mediated gliosis.

Cornelia A Deeg, Barbara Amann, Konstantin Lutz, Sieglinde Hirmer, Karina Lutterberg, Elisabeth Kremmer, Stefanie M Hauck

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  9. Gestational diabetes influences retinal Muller cells in rat's offspring.Iranian journal of basic medical sciences · 2017
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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

7 authors at 3 institutions in 1 country.

Cornelia A DeegExperimental Ophthalmology, Philipps University of Marburg, Baldingerstrasse, 35033, Marburg, Germany. Cornelia.Deeg@uni-marburg.de.
Barbara AmannDepartment of Veterinary Sciences, Institute of Animal Physiology, Ludwig-Maximilians University, Veterinärstr. 13, 80539, München, Germany.
Konstantin LutzDepartment of Veterinary Sciences, Institute of Animal Physiology, Ludwig-Maximilians University, Veterinärstr. 13, 80539, München, Germany.
Sieglinde HirmerDepartment of Veterinary Sciences, Institute of Animal Physiology, Ludwig-Maximilians University, Veterinärstr. 13, 80539, München, Germany.
Karina LutterbergDepartment of Veterinary Sciences, Institute of Animal Physiology, Ludwig-Maximilians University, Veterinärstr. 13, 80539, München, Germany.
Elisabeth KremmerHelmholtz Zentrum München-German Research Center for Environmental Health (GmbH), Institute for Molecular Immunology, Marchioninistraße 25, 81377, München, Germany.
Stefanie M HauckDepartment of Protein Science, Helmholtz Zentrum München-German Research Center for Environmental Health (GmbH), Ingolstädter Landstr. 1, 85764, Neuherberg, Germany.
Ludwig-Maximilians-Universität München · DEHelmholtz Zentrum München · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMüller glial cells are important regulators of physiological function of retina. In a model disease of retinal inflammation and spontaneous recurrent uveitis in horses (ERU), we could show that retinal Müller glial cells significantly change potassium and water channel protein expression during autoimmune pathogenesis. The most significantly changed channel protein in neuroinflammatory ERU was aquaporin 11 (AQP11). Aquaporins (AQP, 13 members) are important regulators of water and small solute transport through membranes. AQP11 is an unorthodox member of this family and was assigned to a third group of AQPs because of its difference in amino acid sequence (conserved sequence is only 11 %) and especially its largely unknown function.

methodsIn order to gain insight into the distribution, localization, and function of AQP11 in the retina, we first developed a novel monoclonal antibody for AQP11 enabling quantification, localization, and functional studies.

resultsIn the horse retina, AQP11 was exclusively expressed at Müller glial cell membranes. In uveitic condition, AQP11 disappeared from gliotic Müller cells concomitant with glutamine synthase. Since function of AQP11 is still under debate, we assessed the impact of AQP11 channel on cell volume regulation of primary Müller glial cells under different osmotic conditions. We conclude a concomitant role for AQP11 with AQP4 in water efflux from these glial cells, which is disturbed in ERU. This could probably contribute to swelling and subsequent severe complication of retinal edema through impaired intracellular fluid regulation.

conclusionsTherefore, AQP11 is important for physiological Müller glia function and the expression pattern and function of this water channel seems to have distinct functions in central nervous system. The significant reduction in neuroinflammation points to a crucial role in pathogenesis of autoimmune uveitis.

Indexed as

AnimalsAquaporinsAutoimmune DiseasesBlotting, WesternEpendymoglial CellsGliosisHorse DiseasesHorsesImmunohistochemistryOsmotic PressureUveitisAquaporinsAQP11AQP4AQP5Autoimmune uveitisCell volume regulationRetinal inflammationSuperaquaporinWater channelWater efflux

Identifiers

PMID27107718
PMCPMC4842293
OpenAlexW2337495045

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.