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Updated: May 28, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

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Transforming Growth Factor beta-2 (TGFβ2) Drives Trabecular Meshwork Progenitor Cell Differentiation Through SMAD2/3

Xiaochen Fan^1,2, Emine K Bilir^1,3, Olivia A Kingston¹

¹Department of Eye and Vision Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool, L69 3BX, UK.

Stem Cells (Dayton, Ohio)

|May 26, 2026

Summary

This summary is machine-generated.

Transforming growth factor beta 2 (TGFβ2) disrupts trabecular meshwork progenitor cell (TMPC) function in primary open-angle glaucoma (POAG). This leads to progenitor depletion and dysfunction, contributing to irreversible blindness from POAG.

Keywords:

TGFβ cell differentiation glaucoma progenitor cells trabecular meshwork

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Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Published on: September 14, 2021

Area of Science:

Ophthalmology
Cell Biology
Regenerative Medicine

Background:

Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness.
Elevated intraocular pressure (IOP) in POAG results from impaired aqueous humor outflow through the trabecular meshwork (TM) and Schlemm's canal.
The mechanisms behind TM tissue maintenance failure and regenerative capacity loss in POAG are not fully understood.

Purpose of the Study:

To investigate the role of transforming growth factor beta 2 (TGFβ2) in regulating trabecular meshwork progenitor cell (TMPC) function.
To determine if elevated TGFβ2 contributes to TM dysfunction and progenitor cell depletion in POAG.
To elucidate the signaling pathways involved in TGFβ2-mediated effects on TMPCs.

Main Methods:

In vitro studies using TMPCs.
Treatment of TMPCs with TGFβ2.
Analysis of gene expression related to TM differentiation and fibrosis.
Assessment of progenitor cell markers.
Inhibition of the TGFβ2-SMAD2/3 signaling pathway.

Main Results:

TGFβ2 treatment induced a fibrotic, differentiated phenotype in TMPCs.
TGFβ2 increased profibrotic gene expression and decreased progenitor cell markers.
The TGFβ2-SMAD2/3 signaling pathway mediated these effects.
Inhibition of this pathway preserved TMPC characteristics and reduced fibrotic gene induction.

Conclusions:

TGFβ2 signaling pathways regulate TMPC fate in vitro.
Elevated TGFβ2 may contribute to POAG pathogenesis by impairing TMPC function and promoting TM fibrosis.
Targeting the TGFβ2-SMAD2/3 pathway could be a potential therapeutic strategy for POAG.