Evidence map›Paper›PMID 27924833›Full record

ArticleScientific reports2016

TGFβ2-induced outflow alterations in a bioengineered trabecular meshwork are offset by a rho-associated kinase inhibitor.

Karen Y Torrejon, Ellen L Papke, Justin R Halman, Magnus Bergkvist, John Danias, Susan T Sharfstein, Yubing Xie

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

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  11. YAP/TAZ Mediate TGFβ2-Induced Schlemm's Canal Cell Dysfunction.Investigative ophthalmology & visual science · 2022
    Article
  12. Review
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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 2 institutions in 1 country.

Karen Y TorrejonColleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 fuller road, Albany, New York, 12203, USA.
Ellen L PapkeColleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 fuller road, Albany, New York, 12203, USA.
Justin R HalmanColleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 fuller road, Albany, New York, 12203, USA.
Magnus BergkvistColleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 fuller road, Albany, New York, 12203, USA.
John DaniasDepartment of Ophthalmology, SUNY Downstate Medical Center, Brooklyn, New York, 11203, USA.
Susan T SharfsteinColleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 fuller road, Albany, New York, 12203, USA.
Yubing XieColleges of Nanoscale Science and Engineering, SUNY Polytechnic Institute, 257 fuller road, Albany, New York, 12203, USA.
SUNY Polytechnic Institute · USSUNY Downstate Health Sciences University · US

Funding

tPA mechanisms in outflow facility regulation in glaucomaR01EY025543 · NEI · SUNY DOWNSTATE MEDICAL CENTER · PI DANIAS, JOHN · 2015 to 2019
$1.8M
Molecular mechanisms in steroid-induced glaucoma.R01EY020670 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CANDIA, OSCAR A, DANIAS, JOHN · 2010 to 2012
$1.5M
NEI NIH HHS R01 EY020670NEI NIH HHS R01 EY025543
6 · The paper itself

Abstract

Members of the transforming growth factor beta (TGFβ) cytokine family have long been associated with affecting several cellular functions, including cell proliferation, differentiation and extracellular matrix (ECM) turnover. Of particular interest to this work, TGFβ2 has been linked to most types of glaucomas as a potential fibrotic agent that can cause elevation of intraocular pressure (IOP). Given that the trabecular meshwork (TM) provides most of aqueous humor outflow resistance in the eye, an in vitro bioengineered human TM (HTM) model has been created and validated by analyzing effects of TGFβ2 on transcellular pressure changes and outflow facility. These changes were correlated with several biological alterations induced by this cytokine, including ECM production and overexpression of HTM-marker myocillin. Furthermore, this TM model has been used to extend current knowledge of gene expression of cytokines involved in TGFβ-induced ECM turnover over time. In particular, the ability for a ROCK-inhibitor to diminish the effect of TGFβ on TM was demonstrated. This work supports the notion that anti-fibrotic activities of ROCK-inhibitors could counteract the elevation of IOP and increased strain observed in glaucomatous TM.

Indexed as

Tissue ScaffoldsActinsalpha-Crystallin B ChainAmidesAnimalsCytoskeletal ProteinsEpoxy CompoundsEye ProteinsGene Expression RegulationGlycoproteinsHumansIntraocular PressureModels, BiologicalMyocilinPerfusionPolymersACTA2 protein, humanActinsalpha-Crystallin B ChainAmidesCRYAB protein, humanCytoskeletal ProteinsEpoxy CompoundsEye ProteinsGlycoproteinsMyocilinPolymersPyridinesrho-Associated KinasesROCK1 protein, humanSU-8 compoundTransforming Growth Factor beta2Y 27632

Identifiers

PMID27924833
PMCPMC5141429
OpenAlexW2560035290

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.