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Related Experiment Video

Updated: Jul 15, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
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Effects of Netarsudil-Family Rho Kinase Inhibitors on Human Trabecular Meshwork Cell Contractility and Actin

Tyler Bagué1, Ayushi Singh1,2, Rajanya Ghosh1

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

Frontiers in Ophthalmology
|July 10, 2024
PubMed
Summary

Netarsudil and related ROCK inhibitors reverse pathological contraction and actin stress fibers in a 3D bioengineered human trabecular meshwork (HTM) model. This study validates a new platform for glaucoma research.

Keywords:
ROCK inhibitionRhopressacytoskeletonprimary open-angle glaucomatissue relaxation

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Area of Science:

  • Ocular Biology
  • Biomaterials Science
  • Pharmacology

Background:

  • Trabecular meshwork (TM) cell and extracellular matrix (ECM) interactions are vital for eye's normal outflow function.
  • Dysregulation of TM contributes to elevated intraocular pressure and glaucoma, characterized by tissue stiffening and actin stress fiber formation.
  • Netarsudil, a Rho-associated kinase inhibitor (ROCKi), is a first-line glaucoma medication that targets TM stiffening.

Purpose of the Study:

  • To investigate the efficacy of netarsudil and related ROCK inhibitors on human TM (HTM) cell contractility and actin remodeling within a 3D ECM environment.
  • To assess the potential of a bioengineered HTM cell-encapsulated ECM hydrogel as a model for studying TM pathophysiology and drug screening.

Main Methods:

  • Development of a bioengineered HTM cell-encapsulated ECM hydrogel model.
  • Treatment of glaucomatous HTM hydrogels with netarsudil and experimental ROCKi compounds.
  • Assessment of ROCK1/2 inhibitory activity, focal adhesion disruption, and reversal of hydrogel contraction and actin stress fibers.

Main Results:

  • Netarsudil and all tested ROCKi compounds demonstrated significant ROCK1/2 inhibition and focal adhesion disruption.
  • All ROCKi compounds dose-dependently reversed pathological HTM hydrogel contraction and actin stress fibers.
  • Netarsudil showed superior performance compared to experimental ROCKi compounds at tailored EC50 levels, validating its clinical status.

Conclusions:

  • Netarsudil effectively rescues HTM cell pathobiology within a 3D tissue-mimetic ECM microenvironment.
  • The bioengineered hydrogel model is a viable platform for screening ROCKi compounds and understanding TM pathophysiology in glaucoma.
  • Further research using this model can advance glaucoma treatment strategies.