Evidence map›Paper›PMID 31035577›Full record

ArticleInternational journal of molecular sciences2019

β-Catenin/Smad3 Interaction Regulates Transforming Growth Factor-β-Induced Epithelial to Mesenchymal Transition in the Lens.

Aftab Taiyab, Julie Holms, Judith A West-Mays

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. RUNX1 promotes NSCLC progression by ACP5/SMAD3-mediated M2 macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  6. Article
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  8. Article
  9. Review
  10. Article
  11. Article
  12. Epithelial-Mesenchymal Transition (EMT).International journal of molecular sciences · 2023
    Article
  13. Article
  14. Article
  15. Advances in interdisciplinary medical and engineering research of intraocular lens surface modifications to prevent posterior capsule opacification.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  16. Article
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  19. 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

3 authors at 1 institution in 1 country.

Aftab TaiyabDepartment of Pathology and Molecular Medicine, McMaster Health Sciences Center, Hamilton, ON L8N 3Z5, Canada. taiyab@mcmaster.ca.
Julie HolmsDepartment of Pathology and Molecular Medicine, McMaster Health Sciences Center, Hamilton, ON L8N 3Z5, Canada. holmsjp@mcmaster.ca.
Judith A West-MaysDepartment of Pathology and Molecular Medicine, McMaster Health Sciences Center, Hamilton, ON L8N 3Z5, Canada. westmayj@mcmaster.ca.ORCID 0000-0003-4293-9131
Hamilton Health Sciences · CA

Funding

Role of MMPs in TGFbeta-induced Cataract FormationR01EY017146 · NEI · MCMASTER UNIVERSITY · PI WEST-MAYS, JUDITH A · 2006 to 2015
$2.2M
National Eye Institute EY017146
6 · The paper itself

Abstract

Cataracts are the leading cause of blindness worldwide. Although surgery is a successful method to restore vision loss due to cataracts, post-surgical complications can occur, such as secondary cataracts, also known as posterior capsular opacification (PCO). PCO arises when lens epithelial cells (LEC) are left behind in the capsular bag following surgery and are induced to undergo epithelial to mesenchymal transition (EMT). Following EMT, LEC morphology and phenotype are altered leading to a loss of transparency and vision. Transforming growth factor (TGF)-β-induced signaling through both canonical, TGF-β/Smad, and non-canonical, β-catenin/Wnt and Rho/ROCK/MRTF-A, pathways have been shown to be involved in lens EMT, and thus PCO. However, the interactions between these signaling pathways in the lens have not been thoroughly explored. In the current study we use rat LEC explants as an ex vivo model, to examine the interplay between three TGF-β-mediated pathways using α-smooth muscle actin (α-SMA) as a molecular marker for EMT. We show that Smad3 inhibition via SIS3 prevents nuclear translocation of β-catenin and MRTF-A, and α-SMA expression, suggesting a key role of Smad3 in regulation of MRTF-A and β-catenin nuclear transport in LECs. Further, we demonstrate that inhibition of β-catenin/CBP interaction by ICG-001 decreased the amount of phosphorylated Smad3 upon TGF-β stimulation in addition to significantly decreasing the expression levels of TGF-β receptors, TBRII and TBRI. Overall, our findings demonstrate interdependence between the canonical and non-canonical TGF-β-mediated signaling pathways controlling EMT in the lens.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsbeta CateninCell NucleusCell ProliferationLens, CrystallineProtein BindingProtein TransportRatsSignal TransductionSmad3 ProteinTransforming Growth Factor betabeta CateninSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor betacataractEMTlensSmad3TGF-ββ-catenin

Identifiers

PMID31035577
PMCPMC6540099
OpenAlexW2941497926

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.