Evidence map›Paper›PMID 22807298›Full record

ArticleInvestigative ophthalmology & visual science2012

Pharmacologic manipulation of conventional outflow facility in ex vivo mouse eyes.

Alexandra Boussommier-Calleja, Jacques Bertrand, David F Woodward, C Ross Ethier, W Daniel Stamer, Darryl R Overby

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

67 citing papers in PubMed, 86 citations in OpenAlex.

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7 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

6 authors at 3 institutions in 2 countries.

Alexandra Boussommier-CallejaDepartment of Bioengineering, Imperial College London, London, UK.
Jacques Bertrand
David F Woodward
C Ross Ethier
W Daniel Stamer
Darryl R Overby
Imperial College London · GBAllergan (United States) · USDuke University · US

Funding

The Mechanical Basis of Primary Open Angle GlaucomaR01EY019696 · NEI · NORTHWESTERN UNIVERSITY · PI FREDBERG, JEFFREY J, JOHNSON, MARK · 2009 to 2019
$7.6M
CADHERIN DYNAMICS AND GLAUCOMAR01EY017007 · NEI · UNIVERSITY OF ARIZONA · PI STAMER, W DANIEL · 2006 to 2010
$1.7M
NEI NIH HHS EY019696NEI NIH HHS EY17007NEI NIH HHS R01 EY017007NEI NIH HHS R01 EY019696
6 · The paper itself

Abstract

purposeMouse models are useful for glaucoma research, but it is unclear whether intraocular pressure (IOP) regulation in mice operates through mechanisms similar to those in humans. Our goal was to determine whether pharmacologic compounds that affect conventional outflow facility in human eyes exert similar effects in C57BL/6 mice.

methodsA computerized perfusion system was used to measure conventional outflow facility in enucleated mouse eyes ex vivo. Paired eyes were perfused sequentially, either immediately after enucleation or after 3 hours storage at 4°C. Three groups of experiments examined sphingosine 1-phosphate (S1P), S1P with antagonists to S1P(1) and S1P(2) receptors, and the prostanoid EP(4) receptor agonist 3,7-dithia PGE(1). We also examined whether a 24-hour postmortem delay affected the response to 3,7-dithia prostaglandin E(1) (PGE(1)).

resultsS1P decreased facility by 39%, and was blocked almost completely by an S1P(2), but not S1P(1), receptor antagonist. The S1P(2) receptor antagonist alone increased facility nearly 2-fold. 3,7-dithia PGE(1) increased facility by 106% within 3 hours postmortem. By 24 hours postmortem, the facility increase caused by 3,7-dithia PGE(1) was reduced 3-fold, yet remained statistically detectable.

conclusionsC57BL/6 mice showed opposing effects of S1P(2) and EP(4) receptor activation on conventional outflow facility, as observed in human eyes. Pharmacologic effects on facility were detectable up to 24 hours postmortem in enucleated mouse eyes. Mice are suitable models to examine the pharmacology of S1P and EP(4) receptor stimulation on IOP regulation as occurs within the conventional outflow pathway of human eyes, and are promising for studying other aspects of aqueous outflow dynamics.

Indexed as

Disease Models, AnimalAlprostadilAnimalsAqueous HumorEye EnucleationFemaleIntraocular PressureLysophospholipidsMaleMiceMice, Inbred C57BLOrgan PreservationReceptors, LysosphingolipidReceptors, Prostaglandin E, EP4 SubtypeSphingosineSphingosine-1-Phosphate Receptors3,7-dithia(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acidAlprostadilLysophospholipidsPtger4 protein, mouseReceptors, LysosphingolipidReceptors, Prostaglandin E, EP4 SubtypeSphingosinesphingosine 1-phosphatesphingosine-1-phosphate receptor-2, mouseSphingosine-1-Phosphate Receptors

Identifiers

PMID22807298
PMCPMC3428113
OpenAlexW2043293171

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.