Evidence map›Paper›PMID 31923415›Full record

ArticleExperimental eye research2020

Nuclear factor-kappa beta signaling is required for transforming growth factor Beta-2 induced ocular hypertension.

Humberto Hernandez, Amanda L Roberts, Colleen M McDowell

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  8. GSK3β Inhibitors Inhibit TGFβ Signaling in the Human Trabecular Meshwork.Investigative ophthalmology & visual science · 2024
    Article
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  18. A20 Attenuates the Fibrotic Response in the Trabecular Meshwork.International journal of molecular sciences · 2022
    Article
  19. Review
  20. Article
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

3 authors at 2 institutions in 1 country.

Humberto HernandezNorth Texas Eye Research Institute, Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA.
Amanda L RobertsNorth Texas Eye Research Institute, Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA.
Colleen M McDowellUniversity of Wisconsin-Madison, Department of Ophthalmology and Visual Sciences, Madison, WI, 53706, USA. Electronic address: cmmcdowell@wisc.edu.
University of North Texas · USUniversity of Wisconsin–Madison · US

Funding

Training in the Neurobiology of Aging and Alzheimer's DiseaseT32AG020494 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI ROBERT Clinton BARBER, NATHALIE SUMIEN · 2002 to 2026
$6.9M
Cross-talk of TGFβ2 and TLR4 in the trabecular meshworkR01EY026529 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI MCDOWELL, COLLEEN MARY · 2016 to 2022
$2.7M
UNT Health Science Center IMSDR25GM125587 · NIGMS · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JONES, HARLAN PIERRE · 2018 to 2022
$1.4M
NEI NIH HHS R01 EY026529NIA NIH HHS T32 AG020494NIGMS NIH HHS R25 GM125587
6 · The paper itself

Abstract

A major risk for the development of primary open-angle glaucoma (POAG) is elevated intraocular pressure (IOP). Elevated IOP is caused by increased outflow resistance due in part to excessive extracellular matrix (ECM) deposition in the trabecular meshwork (TM). The role of transforming growth factor beta 2 (TGFβ2) in inducing ECM production is well understood. Recent studies suggest that toll-like receptor 4 (TLR4) plays an important role in fibrogenesis. We have previously described a crosstalk between TGFβ2 and TLR4 in the development of ocular hypertension and glaucomatous TM damage. Nuclear factor-kappa beta (NF-κB) is critical for TLR4 signaling. To determine the transactivation of NF-κB, TM cells were stimulated with cellular fibronectin containing the EDA isoform (cFN-EDA), TGFβ2, or lipopolysaccharide (LPS) in combination with a selective TLR4 inhibitor. cFN-EDA, TGFβ2, and LPS all induced transactivation of NF-κB and inhibition of TLR4 blocked the effect of each treatment paradigm. To evaluate the role of NF-κB in IOP regulation, we utilized our inducible mouse model of ocular hypertension by injection of Ad5.TGFβ2 in mice harboring a mutation in NF-κB and wild-type controls. IOP was measured over time and eyes accessed by immunohistochemistry for the ECM protein FN and the specific FN-EDA isoform. Ad5.TGFβ2 induced ocular hypertension and expression of FN and FN-EDA in wild-type mice, but mutation in NF-κB blocked the effect. These data suggest that NF-κB is necessary for TGFβ2-induced ECM production and ocular hypertension and the transactivation of NF-κB is dependent on both TGFβ2 and TLR4.

Indexed as

AdenoviridaeAnimalsDisease Models, AnimalExtracellular Matrix ProteinsFibronectinsGenetic VectorsIntraocular PressureMiceMice, Inbred C57BLNF-kappa BOcular HypertensionSignal TransductionToll-Like Receptor 4Tonometry, OcularTrabecular MeshworkTransforming Growth Factor beta2Extracellular Matrix ProteinsFibronectinsNF-kappa BTlr4 protein, mouseToll-Like Receptor 4Transforming Growth Factor beta2GlaucomaMouse modelNF-κBOcular hypertensionTrabecular meshwork

Identifiers

PMID31923415
PMCPMC7015797
OpenAlexW2999636760

What OpenQuestion holds

Textmetadata
LicenceTDM
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.