Evidence map›Paper›PMID 24814605›Full record

ArticleThe American journal of pathology2014

Matrix metalloproteinase-9-null mice are resistant to TGF-β-induced anterior subcapsular cataract formation.

Anna Korol, Giuseppe Pino, Dhruva Dwivedi, Jennifer V Robertson, Paula A Deschamps, Judith A West-Mays

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Transforming growth factor-β in tumour development.Frontiers in molecular biosciences · 2022
    Review
  7. Article
  8. Article
  9. Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  10. Immune cells in lens injury repair and fibrosis.Experimental eye research · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. The role of lipocalin-2 in age-related macular degeneration (AMD).Cellular and molecular life sciences : CMLS · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Matrix metalloproteinase 9 is associated with peritoneal membrane solute transport and induces angiogenesis through β-catenin signaling.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    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

6 authors at 1 institution in 1 country.

Anna KorolDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, Ontario, Canada.
Giuseppe PinoDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, Ontario, Canada.
Dhruva DwivediDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, Ontario, Canada.
Jennifer V RobertsonDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, Ontario, Canada.
Paula A DeschampsDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, Ontario, Canada.
Judith A West-MaysDepartment of Pathology and Molecular Medicine, McMaster University Health Science Centre, Hamilton, Ontario, Canada. Electronic address: westmayj@mcmaster.ca.
McMaster University Medical Centre · CA

Funding

Role of MMPs in TGFbeta-induced Cataract FormationR01EY017146 · NEI · MCMASTER UNIVERSITY · PI WEST-MAYS, JUDITH A · 2006 to 2015
$2.2M
NEI NIH HHS R01 EY017146PHS HHS R01-017146-06
6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is associated with fibrotic diseases in the lens, such as anterior subcapsular cataract (ASC) formation. Often mediated by transforming growth factor (TGF)-β, EMT in the lens involves the transformation of lens epithelial cells into a multilayering of myofibroblasts, which manifest as plaques beneath the lens capsule. TGF-β-induced EMT and ASC have been associated with the up-regulation of two matrix metalloproteinases (MMPs): MMP-2 and MMP-9. The current study used MMP-2 and MMP-9 knockout (KO) mice to further determine their unique roles in TGF-β-induced ASC formation. Adenoviral injection of active TGF-β1 into the anterior chamber of all wild-type and MMP-2 KO mice led to the formation of distinct ASC plaques that were positive for α-smooth muscle actin, a marker of EMT. In contrast, only a small proportion of the MMP-9 KO eyes injected with adenovirus-expressing TGF-β1 exhibited ASC plaques. Isolated lens epithelial explants from wild-type and MMP-2 KO mice that were treated with TGF-β exhibited features indicative of EMT, whereas those from MMP-9 KO mice did not acquire a mesenchymal phenotype. MMP-9 KO mice were further bred onto a TGF-β1 transgenic mouse line that exhibits severe ASC formation, but shows a resistance to ASC formation in the absence of MMP-9. These findings suggest that MMP-9 expression is more critical than MMP-2 in mediating TGF-β-induced ASC formation.

Indexed as

Epithelial-Mesenchymal TransitionActinsAnimalsCadherinsCataractLens Capsule, CrystallineMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mice, KnockoutMice, TransgenicTransforming Growth Factor beta1Acta2 protein, mouseActinsCadherinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, mouseMmp9 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID24814605
PMCPMC4076463
OpenAlexW2138273787

What OpenQuestion holds

Textmetadata
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.