Evidence map›Paper›PMID 34502356›Full record

ArticleInternational journal of molecular sciences2021

Fibrotic Changes to Schlemm's Canal Endothelial Cells in Glaucoma.

Ruth A Kelly, Kristin M Perkumas, Matthew Campbell, G Jane Farrar, W Daniel Stamer, Pete Humphries, Jeffrey O'Callaghan, Colm J O'Brien

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
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  8. Article
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  10. Review
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. YAP/TAZ Mediate TGFβ2-Induced Schlemm's Canal Cell Dysfunction.Investigative ophthalmology & visual science · 2022
    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

8 authors at 3 institutions in 2 countries.

Ruth A KellyOcular Genetics Unit, Smurfit Institute of Genetics, Trinity College Dublin, D02 PN40 Dublin, Ireland.ORCID 0000-0001-8041-4411
Kristin M PerkumasDepartment of Ophthalmology, Duke University Eye Center, Durham, NC 27705, USA.
Matthew CampbellNeurovascular Research Laboratory, Smurfit Institute of Genetics, Trinity College Dublin, D02 PN40 Dublin, Ireland.
G Jane FarrarOcular Genetics Unit, Smurfit Institute of Genetics, Trinity College Dublin, D02 PN40 Dublin, Ireland.
W Daniel StamerDepartment of Ophthalmology, Duke University Eye Center, Durham, NC 27705, USA.
Pete HumphriesOcular Genetics Unit, Smurfit Institute of Genetics, Trinity College Dublin, D02 PN40 Dublin, Ireland.
Jeffrey O'CallaghanOcular Genetics Unit, Smurfit Institute of Genetics, Trinity College Dublin, D02 PN40 Dublin, Ireland.
Colm J O'BrienDepartment of Ophthalmology, Mater Misericordiae University Hospital, D07 AX57 Dublin, Ireland.
Trinity College Dublin · IEDuke University · USMater Misericordiae University Hospital · IE

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
eNOS-Dependent Mechanoregulation of Intraocular PressureR01EY022359 · NEI · DUKE UNIVERSITY · PI STAMER, W DANIEL · 2012 to 2025
$5.6M
European Research Council ERC-2012-AdGNEI NIH HHS P30 EY005722NEI NIH HHS R01 EY022359Science Foundation Ireland SFI: 16/1A/4452; 18/TIDA/6120
6 · The paper itself

Abstract

Previous studies have shown that glaucomatous Schlemm's canal endothelial cells (gSCECs) are stiffer and associated with reduced porosity and increased extracellular matrix (ECM) material compared to SCECs from healthy individuals. We hypothesised that Schlemm's canal (SC) cell stiffening was a function of fibrotic changes occurring at the inner wall of SC in glaucoma. This study was performed in primary cell cultures isolated from the SC lumen of human donor eyes. RNA and protein quantification of both fibrotic and endothelial cell markers was carried out on both healthy and gSCECs. Functional assays to assess cell density, size, migration, proliferation, and mitochondrial function of these cells were also carried out. Indeed, we found that gSCECs deviate from typical endothelial cell characteristics and exhibit a more fibrotic phenotype. For example, gSCECs expressed significantly higher protein levels of the fibrotic markers α-SMA, collagen I-α1, and fibronectin, as well as significantly increased protein expression of TGFβ-2, the main driver of fibrosis, compared to healthy SCECs. Interestingly, we observed a significant increase in protein expression of endothelial marker VE-cadherin in gSCECs, compared to healthy SCECs. gSCECs also appeared to be significantly larger, and surprisingly proliferate and migrate at a significantly higher rate, as well as showing significantly reduced mitochondrial activity, compared to healthy SCECs.

Indexed as

Antigens, CDAqueous HumorCadherin 5CadherinsCell CountCell MovementCell ProliferationEndothelial CellsEndotheliumExtracellular MatrixEyeFibrosisGlaucomaHumansMitochondriaPorosityAntigens, CDCadherin 5CadherinsTransforming Growth Factor beta2endothelial cellsendothelial–mesenchymal transitionfibrosisglaucomaproliferationSchlemm’s canal

Identifiers

PMID34502356
PMCPMC8431431
OpenAlexW3198024241

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.