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

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...

You might also read

Related Articles

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

Sort by
Same author

Microtubule stability modulates Schlemm's canal cell mechanobiology and outflow facility in glaucoma.

bioRxiv : the preprint server for biology·2026
Same author

Surgical menopause impact on vaginal mechanical properties.

Journal of biomechanics·2026
Same author

Segmental outflow and trabecular meshwork stiffness in an ocular hypertensive mouse model.

bioRxiv : the preprint server for biology·2026
Same author

Author Response: Scientific Concerns About Recent Fluid-Structure Interaction Models of the Aqueous Humor Outflow Pathway.

Investigative ophthalmology & visual science·2026
Same author

Endothelial cell stiffness and type drive the formation of biomechanically induced transcellular pores.

Cell reports·2025
Same author

Scientific Concerns About Recent Fluid-Structure Interaction Models of the Aqueous Humor Outflow Pathway.

Investigative ophthalmology & visual science·2025

Related Experiment Video

Updated: Jun 26, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
09:03

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

Segmental Outflow and Trabecular Meshwork Stiffness in an Ocular Hypertensive Mouse Model.

Cydney A Wong1,2, A Thomas Read1, Guorong Li3

  • 1Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia, United States.

Investigative Ophthalmology & Visual Science
|June 25, 2026
PubMed
Summary

Dexamethasone (DEX) elevates intraocular pressure (IOP) in mice by altering trabecular meshwork (TM) flow, not by changing TM stiffness. Subtle structural changes in low-flow regions may contribute to steroid-induced glaucoma.

More Related Videos

A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects
07:00

A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects

Published on: August 14, 2013

Related Experiment Videos

Last Updated: Jun 26, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
09:03

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects
07:00

A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects

Published on: August 14, 2013

Area of Science:

  • Ophthalmology
  • Biomedical Engineering
  • Cell Biology

Background:

  • Elevated intraocular pressure (IOP) is a primary risk factor for primary open-angle glaucoma (POAG).
  • Trabecular meshwork (TM) outflow is segmental, with distinct high-flow (HF) and low-flow (LF) regions.
  • Understanding how ocular hypertension affects these regions is crucial for glaucoma research.

Purpose of the Study:

  • To investigate the impact of ocular hypertension on segmental outflow in a dexamethasone (DEX)-induced mouse model.
  • To compare trabecular meshwork (TM) stiffness between HF and LF regions in response to DEX treatment.
  • To characterize TM structural and mechanical changes in steroid-induced ocular hypertension.

Main Methods:

  • DEX or vehicle nanoparticles were injected into C57BL/6J mice over 4 weeks, with weekly IOP measurements.
  • In vivo perfusion with fluorescent nanospheres assessed segmental flow patterns (HF, intermediate-flow, LF regions).
  • Atomic force microscopy measured TM stiffness; immunofluorescence analyzed fibronectin and alpha-smooth muscle actin levels.

Main Results:

  • DEX treatment significantly increased IOP by 33.3% and altered tracer distribution.
  • No significant differences in TM stiffness were found between DEX-treated and control mice, or between HF and LF regions.
  • Increased fibronectin in LF regions of DEX-treated eyes suggested subtle TM structural changes not detected by AFM.

Conclusions:

  • DEX alters segmental flow distribution, potentially impacting cell contractility rather than extracellular matrix stiffness, leading to IOP elevation in young mice.
  • These findings enhance our understanding of segmental outflow dynamics and TM mechanics in steroid-induced glaucoma.
  • The study highlights potential mechanisms of IOP elevation relevant to glaucoma pathogenesis.