Evidence map›Paper›PMID 41696446›Full record

ArticleFrontiers in cell and developmental biology2025

A switch from α5β1 to αvβ3 integrin activity contributes to the development of a profibrotic mesenchymal phenotype in trabecular meshwork cells.

Kassidy L Johns, Jennifer A Faralli, Mark S Filla, Nandini Shah, Kate E Keller, Donna M Peters

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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.

Kassidy L JohnsDepartment of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.
Jennifer A FaralliDepartment of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.
Mark S FillaDepartment of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.
Nandini ShahDepartment of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.
Kate E KellerCasey Eye Institute, Oregon Health & Science University, Portland, OR, United States.
Donna M PetersDepartment of Pathology & Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Proteomics CoreP30EY010572 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI John Peter Campbell · 1995 to 2026
$19.4M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI AKIHIRO IKEDA · 2005 to 2026
$12.6M
Control of Trabecular Meshwork CytoskeletonR01EY017006 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI PETERS, DONNA M · 2006 to 2024
$6.1M
Extracellular Matrix and Outflow ResistanceR01EY019643 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI KELLER, KATE E · 2010 to 2025
$5.0M
NFAT and fibrosis in the trabecular meshworkR01EY032905 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI PETERS, DONNA M · 2022 to 2025
$1.7M
Thrombospondin-1 in normal and glaucomatous trabecular meshworkR01EY032590 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI KELLER, KATE E · 2022 to 2025
$1.6M
Automated Tissue MicroarrayerS10OD023526 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI MATKOWSKYJ, KRISTINA A. · 2018 to 2018
$184k
NCI NIH HHS P30 CA014520NEI NIH HHS P30 EY010572NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY017006NEI NIH HHS R01 EY019643NEI NIH HHS R01 EY032590NEI NIH HHS R01 EY032905NIH HHS S10 OD023526
6 · The paper itself

Abstract

Purpose: Fibrogenic changes in the trabecular meshwork (TM) are considered to be a major cause for the restriction in aqueous humor outflow from the anterior chamber associated with primary open angle glaucoma. In this study, we investigated whether integrin switching from α5β1 to αvβ3 integrin expression could initiate fibrotic-like changes in the TM that could restrict outflow. Methods: Human TM cells were isolated from young (<40 years) and old (>50 years) donor eyes. RT-PCR, western blots and immunofluorescence microscopy were used to evaluate levels of integrin and αSMA expression. Lentiviral shRNA vectors were used to knockdown α5 and β3 integrin levels. Paraffin embedded anterior segments of young and old donor eyes were used to evaluate αSMA levels Results: Studies revealed an age-related decrease in α5 integrin mRNA expression in TM cells. This loss was accompanied by an increase in αSMA mRNA and protein levels and an increase in activated αvβ3 integrin levels. Knockdown of β3 integrin mRNA and protein levels decreased the expression of αSMA mRNA and protein levels. Elevated mRNA levels of the EndMT biomarkers, Conclusion: These studies suggest that crosstalk between α5β1 and αvβ3 integrin signaling controls expression of αSMA mRNA and protein levels and that β3 integrins may play a role in the development of the fibrogenic phenotype in TM cells and associated with POAG.

Indexed as

agingcontractilityEndMTintegrinstrabecular meshwork

Identifiers

PMID41696446
PMCPMC12901422

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Registered trials

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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.