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Related Concept Videos

Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...

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Related Experiment Video

Updated: Jun 18, 2026

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
13:47

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Cytoskeletal changes in cultured human glaucoma trabecular meshwork cells.

A F Clark1, S T Miggans, K Wilson

  • 1Alcon Laboratories, Fort Worth, Texas, U.S.A.

Journal of Glaucoma
|November 19, 2009
PubMed
Summary

Glaucoma patient trabecular meshwork (TM) cells show increased cross-linked actin networks (CLANs), especially after glucocorticoid exposure. This suggests CLANs may contribute to ocular hypertension in glaucoma.

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Last Updated: Jun 18, 2026

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In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma

Published on: May 11, 2015

Area of Science:

  • Ocular biology
  • Cellular biophysics
  • Glaucoma research

Background:

  • Glucocorticoid treatment alters trabecular meshwork (TM) cell function and actin microfilaments.
  • Cross-linked actin networks (CLANs) are a key structural change induced by glucocorticoids in TM cells.

Purpose of the Study:

  • To investigate if glaucoma patient-derived TM cells exhibit similar microfilament structural changes.
  • To determine the effect of glucocorticoids on CLAN formation in glaucoma TM cells.

Main Methods:

  • Examined microfilament structures in nine TM cell cultures (four glaucoma, five normal) using epifluorescent and transmission electron microscopy.
  • Cultured cells with and without dexamethasone (DEX) for 7-14 days.

Main Results:

  • Glaucoma TM cell lines (TM23, TM36C, TM48D) exhibited high CLAN levels without DEX, unlike normal cells and TM13.
  • Dexamethasone significantly increased CLAN expression in all tested TM cell lines, both normal and glaucomatous.

Conclusions:

  • Elevated CLAN formation in glaucoma TM cells, particularly with glucocorticoid exposure, is a potential factor in ocular hypertension.
  • Understanding CLANs in TM cells could offer insights into glaucoma pathogenesis.