Evidence map›Paper›PMID 28400560›Full record

ArticleScientific reports2017

TGF-β induces phosphorylation of phosphatase and tensin homolog: implications for fibrosis of the trabecular meshwork tissue in glaucoma.

Nikoleta Tellios, Jillian C Belrose, Alexander C Tokarewicz, Cindy Hutnik, Hong Liu, Andrew Leask, Michael Motolko, Miho Iijima, Sunil K Parapuram

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

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  16. Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021
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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

9 authors at 4 institutions in 2 countries.

Nikoleta TelliosDepartment of Ophthalmology, University of Western Ontario, London, ON, N6A 4V2, Canada.
Jillian C BelroseDepartment of Ophthalmology, University of Western Ontario, London, ON, N6A 4V2, Canada.
Alexander C TokarewiczDepartment of Ophthalmology, University of Western Ontario, London, ON, N6A 4V2, Canada.
Cindy HutnikDepartment of Ophthalmology, University of Western Ontario, London, ON, N6A 4V2, Canada.
Hong LiuLawson Health Research Institute, St. Joseph's Health Care, London, ON, N6A 4V2, Canada.
Andrew LeaskDentistry, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, N6A 5C1, Canada.
Michael MotolkoDepartment of Ophthalmology, University of Western Ontario, London, ON, N6A 4V2, Canada.
Miho IijimaDepartment of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Sunil K ParapuramDepartment of Ophthalmology, University of Western Ontario, London, ON, N6A 4V2, Canada. sparapur@uwo.ca.
Western University · CAJohns Hopkins Medicine · USLawson Health Research Institute · CASt Joseph's Health Care · CA

Funding

Lipid Signaling in ChemotaxisR01GM084015 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI IIJIMA, MIHO · 2009 to 2019
$2.9M
NIGMS NIH HHS R01 GM084015
6 · The paper itself

Abstract

Fundamental cell signaling mechanisms that regulate dynamic remodeling of the extracellular matrix (ECM) in mechanically loaded tissues are not yet clearly understood. Trabecular meshwork (TM) tissue in the eye is under constant mechanical stress and continuous remodeling of ECM is crucial to maintain normal aqueous humor drainage and intraocular pressure (IOP). However, excessive ECM remodeling can cause fibrosis of the TM as in primary open-angle glaucoma (POAG) patients, and is characterized by increased resistance to aqueous humor drainage, elevated IOP, optic nerve degeneration and blindness. Increased levels of active transforming growth factor-β2 (TGF-β2) in the aqueous humor is the main cause of fibrosis of TM in POAG patients. Herein, we report a novel finding that, in TM cells, TGF-β-induced increase in collagen expression is associated with phosphorylation of phosphatase and tensin homolog (PTEN) at residues Ser380/Thr382/383. Exogenous overexpression of a mutated form of PTEN with enhanced phosphatase activity prevented the TGF-β-induced collagen expression by TM cells. We propose that rapid alteration of PTEN activity through changes in its phosphorylation status could uniquely regulate the continuous remodeling of ECM in the normal TM. Modulating PTEN activity may have high therapeutic potential to alleviating the fibrosis of TM in POAG patients.

Indexed as

Protein Processing, Post-TranslationalCells, CulturedCollagenExtracellular MatrixFibrosisGlaucoma, Open-AngleHumansPhosphorylationPTEN PhosphohydrolaseTrabecular MeshworkTransforming Growth Factor betaCollagenPTEN PhosphohydrolasePTEN protein, humanTransforming Growth Factor beta

Identifiers

PMID28400560
PMCPMC5429747
OpenAlexW2604797828

What OpenQuestion holds

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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.