Evidence map›Paper›PMID 36139071›Full record

ArticleBiomolecules2022

Fibrotic Response of Human Trabecular Meshwork Cells to Transforming Growth Factor-Beta 3 and Autotaxin in Aqueous Humor.

Mengxuan Liu, Megumi Honjo, Reiko Yamagishi, Nozomi Igarashi, Natsuko Nakamura, Makoto Kurano, Yutaka Yatomi, Koji Igarashi, Makoto Aihara

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
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 5 institutions in 1 country.

Mengxuan LiuDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Megumi HonjoDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Reiko YamagishiDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Nozomi IgarashiDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-2275-6285
Natsuko NakamuraDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Makoto KuranoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Yutaka YatomiDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Koji IgarashiBioscience Division, Reagent Development Department, AIA Research Group, TOSOH Corporation, Ayaseshi 252-1123, Japan.ORCID 0000-0002-5007-7079
Makoto AiharaDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0001-6810-0583
The University of Tokyo · JPUniversity of Tokyo Hospital · JPTokyo Medical Center · JPTokyo Teishin Hospital · JPTosoh (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study examines the potential role of transforming growth factor-beta 3 (TGF-β3) on the fibrotic response of cultured human trabecular meshwork (HTM) cells. The relationships and trans-signaling interactions between TGF-β3 and autotaxin (ATX) in HTM cells were also examined. The levels of TGF-β and ATX in the aqueous humor (AH) of patients were measured by an immunoenzymetric assay. The TGF-β3-induced expression of the fibrogenic markers, fibronectin, collagen type I alpha 1 chain, and alpha-smooth muscle actin, and ATX were examined by quantitative real-time PCR, Western blotting, and immunocytochemistry, and the trans-signaling regulatory effect of TGF-β3 on ATX expression was also evaluated. In HTM cells, the significant upregulation of ATX was induced by TGF-β3 at a concentration of 0.1 ng/mL, corresponding to the physiological concentration in the AH of patients with exfoliative glaucoma (XFG). However, higher concentrations of TGF-β3 significantly suppressed ATX expression. TGF-β3 regulated ATX transcription and signaling in HTM cells, inducing the upregulation of fibrogenic proteins in a dose-dependent manner. Trans-signaling of TGF-β3 regulated ATX transcription, protein expression, and signaling, and was thereby suggested to induce fibrosis of the trabecular meshwork. Modulation of trans-signaling between TGF-β3 and ATX may be key to elucidate the pathology of XFG, and for the development of novel treatment modalities.

Indexed as

Aqueous HumorPhosphoric Diester HydrolasesTrabecular MeshworkTransforming Growth Factor beta3ActinsCells, CulturedCollagen Type IFibronectinsFibrosisHumansLysophospholipase DActinsCollagen Type IFibronectinsLysophospholipase DPhosphoric Diester HydrolasesTGFB3 protein, humanTransforming Growth Factor beta3autotaxinhuman trabecular meshwork cellstransforming growth factor-beta 3

Identifiers

PMID36139071
PMCPMC9496180
OpenAlexW4294989818

What OpenQuestion holds

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Registered trials

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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.