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TGF - β Signaling Pathway

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...

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Related Experiment Video

Updated: Aug 22, 2025

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

YAP/TAZ Mediate TGFβ2-Induced Schlemm's Canal Cell Dysfunction.

Haiyan Li^1,2, Ayushi Singh^1,2, Kristin M Perkumas³

¹Department of Ophthalmology and Visual Sciences, SUNY Upstate Medical University, Syracuse, New York, United States.

Investigative Ophthalmology & Visual Science

|November 9, 2022

Summary

This summary is machine-generated.

Elevated TGFβ2 in glaucoma disrupts Schlemm

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Last Updated: Aug 22, 2025

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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Area of Science:

Ocular Biology
Cellular Mechanotransduction
Glaucoma Pathophysiology

Background:

Elevated transforming growth factor beta2 (TGFβ2) in aqueous humor is associated with glaucomatous outflow tissue dysfunction.
Yes-associated protein (YAP) and transcriptional coactivator with PDZ binding motif (TAZ) are potential mediators of this dysfunction.
The precise mechanisms of YAP/TAZ regulation in Schlemm's canal (SC) cells under glaucomatous conditions remain unclear.

Purpose of the Study:

To investigate how TGFβ2 modulates YAP/TAZ activity in human SC (HSC) cells.
To examine the potential of pharmacological YAP/TAZ inhibition to counteract TGFβ2-induced HSC cell dysfunction.

Main Methods:

HSC cells were cultured on or within biomimetic extracellular matrix hydrogels.
Cells were treated with TGFβ2, with or without actin destabilization or YAP/TAZ inhibition (verteporfin).
Assessed changes in actin cytoskeleton, YAP/TAZ nuclear localization, extracellular matrix production, and hydrogel contraction.

Main Results:

TGFβ2 increased YAP/TAZ nuclear localization in HSC cells, which was mitigated by actin cytoskeleton modulation.
Verteporfin treatment reduced fibronectin expression and actomyosin rearrangement induced by TGFβ2.
Pharmacological YAP/TAZ inhibition attenuated TGFβ2-induced hydrogel contraction by HSC cells.

Conclusions:

Aberrant YAP/TAZ signaling plays a pathological role in HSC cells under simulated glaucomatous conditions.
Pharmacological YAP/TAZ inhibition shows promise for treating outflow tissue dysfunction in glaucoma.
Targeting YAP/TAZ signaling may offer a novel therapeutic strategy for glaucoma management.