Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Glaucoma: Overview01:25

Glaucoma: Overview

1.6K
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...
1.6K
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

1.1K
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...
1.1K
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

1.5K
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
1.5K
Formation of Higher-order Actin Filaments01:11

Formation of Higher-order Actin Filaments

3.7K
The polymerization of G-actin monomers into filamentous F-actin is a multi-step process. Once the F-actins are formed, they can bundle together in different arrangements to form higher-order networks and regulate cellular functions. Common examples include the formation of lamellipodia and filopodia at the cell's leading edge by actin reorganization in a migrating cell. The microvilli on the brush border epithelial cells are also formed through the F-actin network.
The high-order actin...
3.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration.

Molecular neurodegeneration·2026
Same author

Cross-linked actin networks (CLANs) and their role in the trabecular meshwork.

Experimental eye research·2026
Same author

GrapheneChat: A Large Language Model for Enhancing Graphene Research.

ACS nano·2026
Same author

Patient-Reported Symptoms Versus Clinician-Measured Signs to Distinguish Sjogren's in Patients With Dry Eye.

Translational vision science & technology·2026
Same author

Mechanistic Insights into Glucocorticoid-Induced Ocular Hypertension Using Differences in Mouse Strain Responsiveness.

The American journal of pathology·2025
Same author

Therapeutic mRNA delivery of CRISPR-Cas9 to the trabecular meshwork reverses ocular hypertension in myocilin glaucoma.

Molecular therapy. Methods & clinical development·2025

Related Experiment Video

Updated: Mar 7, 2026

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

2.0K

Cross-linked actin networks (CLANs) in glaucoma.

Jaclyn Y Bermudez1, Michela Montecchi-Palmer1, Weiming Mao1

  • 1North Texas Eye Research Institute, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107, United States.

Experimental Eye Research
|February 28, 2017
PubMed
Summary

Glaucoma causes vision loss by increasing intraocular pressure (IOP). Cross-linked actin networks (CLANs) in the trabecular meshwork (TM) contribute to IOP elevation, and understanding their regulation may offer new glaucoma treatments.

Keywords:
Cross-linked actin networksGlaucomaGlucocorticoidsTGFβ2Trabecular meshwork

More Related Videos

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
08:55

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

3.5K
In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
12:48

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

Published on: May 11, 2015

11.2K

Related Experiment Videos

Last Updated: Mar 7, 2026

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

2.0K
Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
08:55

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

3.5K
In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
12:48

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

Published on: May 11, 2015

11.2K

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Biochemistry

Background:

  • Glaucoma is a leading cause of irreversible blindness worldwide.
  • Elevated intraocular pressure (IOP) is a major risk factor for glaucoma, but its molecular mechanisms are not fully understood.
  • The trabecular meshwork (TM) is crucial for regulating IOP; its dysfunction leads to elevated IOP.

Purpose of the Study:

  • To investigate the role of cross-linked actin networks (CLANs) in the trabecular meshwork (TM) in elevated intraocular pressure (IOP).
  • To explore the mechanisms by which glucocorticoids (GCs) and TGFβ2 induce CLAN formation in TM cells.
  • To understand the regulation of CLANs by signaling pathways for potential novel glaucoma therapies.

Main Methods:

  • Induction of CLANs in confluent TM cells and TM tissues using glucocorticoids (GCs) and TGFβ2.
  • Analysis of cytoskeletal rearrangements and extracellular matrix deposition in glaucomatous TM.
  • Investigation of signaling pathways involved in CLAN formation.

Main Results:

  • Glaucomatous TM exhibits increased extracellular matrix deposition and CLANs.
  • CLANs, characterized by dome-like structures, are associated with increased aqueous humor outflow resistance and IOP.
  • CLANs are inducible by GCs and TGFβ2 in TM cells and tissues.

Conclusions:

  • CLANs contribute to increased IOP by stiffening TM cells and tissue.
  • Understanding CLAN induction and regulation by GCs and TGFβ2 is crucial.
  • Targeting CLANs may offer novel therapeutic strategies for preventing or intervening in glaucomatous damage to the TM.