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TGFbeta2-induced changes in human trabecular meshwork: implications for intraocular pressure.

Debra L Fleenor¹, Allan R Shepard, Peggy E Hellberg

¹Glaucoma Research, Alcon Research, Ltd., Fort Worth, Texas 76134, USA. debra.fleenor@alconlabs.com

Investigative Ophthalmology & Visual Science

|December 31, 2005

Summary

Transforming growth factor-beta2 (TGFbeta2) elevates intraocular pressure (IOP) by increasing extracellular matrix (ECM) components like fibronectin and plasminogen activator inhibitor-1 (PAI-1) in the trabecular meshwork (TM). Targeting TGFbeta2 may offer new glaucoma treatments.

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Area of Science:

Ophthalmology
Cell Biology
Molecular Biology

Background:

Elevated transforming growth factor-beta2 (TGFbeta2) in glaucomatous aqueous humor suggests a role in disease pathogenesis.
Excess extracellular matrix (ECM) in the trabecular meshwork (TM) may increase aqueous outflow resistance, contributing to glaucoma.

Purpose of the Study:

To investigate the effects of TGFbeta2 on fibronectin and plasminogen activator inhibitor-1 (PAI-1) secretion in human TM cells.
To determine TGFbeta2's impact on intraocular pressure (IOP) and ECM component levels in perfused human anterior segments.

Main Methods:

Gene microarray analysis of human TM cell monolayers treated with TGFbeta2.
ELISA to quantify fibronectin and PAI-1 in TM cell supernatants and anterior segment eluates.

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Perfusion organ culture model of human anterior segments to assess TGFbeta2 effects on IOP.

Main Results:

TGFbeta2 upregulated ECM-related genes, including PAI-1, in TM cells.
TGFbeta2 increased fibronectin and PAI-1 secretion from TM cells, effects blocked by TGFbeta type I receptor inhibitors.
In perfused anterior segments, TGFbeta2 elevated IOP and increased fibronectin and PAI-1 in eluates.

Conclusions:

TGFbeta2 influences IOP via TGFbeta type I receptor-mediated modulation of TM ECM secretion.
Targeting TGFbeta2-induced ECM changes presents a potential therapeutic strategy for glaucoma management.