Evidence map›Paper›PMID 28209733›Full record

ArticleMolecular biology of the cell2017

Dual function of TGFβ in lens epithelial cell fate: implications for secondary cataract.

Bruce A Boswell, Anna Korol, Judith A West-Mays, Linda S Musil

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. ErbBs in Lens Cell Fibrosis and Secondary Cataract.Investigative ophthalmology & visual science · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  17. Article
  18. Article
  19. Article
  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

4 authors at 2 institutions in 2 countries.

Bruce A BoswellDepartment of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, OR 97239.
Anna KorolDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, ON L8N 3Z5, Canada.
Judith A West-MaysDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, ON L8N 3Z5, Canada.
Linda S MusilDepartment of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, OR 97239 musill@OHSU.edu.
McMaster University Medical Centre · CAOregon Health & Science University · US

Funding

Oregon Clinical and Translational Research InstituteUL1TR000128 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI ELLISON, DAVID H · 2012 to 2015
$28.7M
Role of MMPs in TGFbeta-induced Cataract FormationR01EY017146 · NEI · MCMASTER UNIVERSITY · PI WEST-MAYS, JUDITH A · 2006 to 2015
$2.2M
TGFB signaling as a therapeutic target in cataract and PCOR01EY022113 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI MUSIL, LINDA S · 2012 to 2014
$1.1M
NCATS NIH HHS UL1 TR000128NEI NIH HHS R01 EY017146NEI NIH HHS R01 EY022113
6 · The paper itself

Abstract

The most common vision-disrupting complication of cataract surgery is posterior capsule opacification (PCO; secondary cataract). PCO is caused by residual lens cells undergoing one of two very different cell fates: either transdifferentiating into myofibroblasts or maturing into lens fiber cells. Although TGFβ has been strongly implicated in lens cell fibrosis, the factors responsible for the latter process have not been identified. We show here for the first time that TGFβ can induce purified primary lens epithelial cells within the same culture to undergo differentiation into either lens fiber cells or myofibroblasts. Marker analysis confirmed that the two cell phenotypes were mutually exclusive. Blocking the p38 kinase pathway, either with direct inhibitors of the p38 MAP kinase or a small-molecule therapeutic that also inhibits the activation of p38, prevented TGFβ from inducing epithelial-myofibroblast transition and cell migration but did not prevent fiber cell differentiation. Rapamycin had the converse effect, linking MTOR signaling to induction of fiber cell differentiation by TGFβ. In addition to providing novel potential therapeutic strategies for PCO, our findings extend the so-called TGFβ paradox, in which TGFβ can induce two disparate cell fates, to a new epithelial disease state.

Indexed as

AnimalsCell DifferentiationCell MovementCell ProliferationChick EmbryoEpithelial CellsEpitheliumEye ProteinsHumansLens, CrystallineMyofibroblastsSignal TransductionTransforming Growth Factor betaEye ProteinsTransforming Growth Factor beta

Identifiers

PMID28209733
PMCPMC5385940
OpenAlexW2588786207

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.