Evidence map›Paper›PMID 27976512›Full record

ArticleJournal of cellular and molecular medicine2017

FGF2 antagonizes aberrant TGFβ regulation of tropomyosin: role for posterior capsule opacity.

Eri Kubo, Shinsuke Shibata, Teppei Shibata, Etsuko Kiyokawa, Hiroshi Sasaki, Dhirendra P Singh

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  7. Consilience and unity in ocular anterior segment research.International journal of ophthalmology · 2024
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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

6 authors at 2 institutions in 2 countries.

Eri KuboDepartment of Ophthalmology, Kanazawa Medical University, Uchinada, Kahoku-gun, Ishikawa, Japan.
Shinsuke ShibataDepartment of Ophthalmology, Kanazawa Medical University, Uchinada, Kahoku-gun, Ishikawa, Japan.
Teppei ShibataDepartment of Ophthalmology, Kanazawa Medical University, Uchinada, Kahoku-gun, Ishikawa, Japan.
Etsuko KiyokawaDepartment of Oncogenic Pathology, Kanazawa Medical University, Uchinada, Kahoku-gun, Ishikawa, Japan.
Hiroshi SasakiDepartment of Ophthalmology, Kanazawa Medical University, Uchinada, Kahoku-gun, Ishikawa, Japan.
Dhirendra P SinghDepartment of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE, USA.
Kanazawa Medical University · JPUniversity of Nebraska Medical Center · US

Funding

Regulation and Function of Prdx6 in eye lens during Aging & Oxidative StressR01EY024589 · NEI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SINGH, DHIRENDRA P · 2014 to 2018
$1.9M
NEI NIH HHS R01 EY024589
6 · The paper itself

Abstract

Transforming growth factor (TGF) β2 and fibroblast growth factor (FGF) 2 are involved in regulation of posterior capsule opacification (PCO) and other processes of epithelial-mesenchymal transition (EMT) such as cancer progression, wound healing and tissue fibrosis as well as normal embryonic development. We previously used an in vivo rodent PCO model to show the expression of tropomyosin (Tpm) 1/2 was aberrantly up-regulated in remodelling the actin cytoskeleton during EMT. In this in vitro study, we show the Tpms family of cytoskeleton proteins are involved in regulating and stabilizing actin microfilaments (F-actin) and are induced by TGFβ2 during EMT in lens epithelial cells (LECs). Importantly, we found TGFβ2 and FGF2 played contrasting roles. Stress fibre formation and up-regulation of α-smooth muscle actin (αSMA) induced by TGFβ2 could be reversed by Tpm1/2 knock-down by siRNA. Expression of Tpm1/2 and stress fibre formation induced by TGFβ2 could be reversed by FGF2. Furthermore, FGF2 delivery to TGFβ-treated LECs perturbed EMT by reactivating the mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) pathway and subsequently enhanced EMT. Conversely, MEK inhibitor (PD98059) abated the FGF2-mediated Tpm1/2 and αSMA suppression. However, we found that normal LECs which underwent EMT showed enhanced migration in response to combined TGFβ and FGF2 stimulation. These findings may help clarify the mechanism reprogramming the actin cytoskeleton during morphogenetic EMT cell proliferation and fibre regeneration in PCO. We propose that understanding the physiological link between levels of FGF2, Tpm1/2 expression and TGFβs-driven EMT orchestration may provide clue(s) to develop therapeutic strategies to treat PCO based on Tpm1/2.

Indexed as

ActinsAnimalsBiomarkersCapsule OpacificationCell MovementCell ShapeEpithelial CellsEpithelial-Mesenchymal TransitionFibroblast Growth Factor 2HumansLens Capsule, CrystallineMAP Kinase Signaling SystemMice, Inbred BALB CPhenotypeRNA, Small InterferingTransfectionActinsBiomarkersFibroblast Growth Factor 2RNA, Small InterferingTransforming Growth Factor beta2Tropomyosinepithelial-mesenchymal transitionFGF2lens epithelial cellsTGFβ2tropomyosin

Identifiers

PMID27976512
PMCPMC5387175
OpenAlexW2565662091

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.