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Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
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Mechano- and Glucocorticoid-Sensitive TREK-1 Channels Regulate Conventional Outflow and Intraocular Pressure
Sarah N Redmon1, Oleg Yarishkin1, Christopher N Rudzitis1,2
1Department of Ophthalmology and Visual Sciences, University of Utah School of Medicine, Salt Lake City, Utah, United States.
Investigative Ophthalmology & Visual Science
|November 21, 2025
Summary
Corticosteroids can impair TREK-1 function in the trabecular meshwork, potentially affecting intraocular pressure (IOP). Activating TREK-1 may help lower IOP in steroid-induced ocular hypertension.
Area of Science:
- Ophthalmology
- Molecular Biology
- Physiology
Background:
- Corticosteroids are widely used but can cause ocular hypertension (OHT).
- The trabecular meshwork (TM) regulates aqueous humor outflow and intraocular pressure (IOP).
- Mechanosensitive ion channels, like TREK-1, play roles in cellular function and pressure regulation.
Purpose of the Study:
- To investigate the molecular link between corticosteroid exposure and mechanosensation.
- To determine the role of the mechanosensitive TWIK-related potassium channel-1 (TREK-1) in aqueous humor outflow regulation.
- To establish TREK-1's role in corticosteroid-induced ocular hypertension (OHT).
Main Methods:
- Real-time PCR to analyze gene expression in mouse TM cells.
- Immunohistochemistry for TREK-1 localization.
- iPerfusion and tonometry in mouse models.
- Whole-cell recording in human TM cells.
- Telemetry in rat models.
Main Results:
- Dexamethasone (DEX) suppressed TREK-1 (Kcnk2) mRNA expression in mouse TM cells.
- TREK-1 agonist ML-402 increased outflow facility and reduced IOP in mouse and rat models.
- Chronic DEX exposure altered human TM cell function and TREK-1 currents.
Conclusions:
- Corticosteroid overexposure may disrupt IOP homeostasis by impairing TM TREK-1 expression and function.
- Pharmacological activation of TREK-1 shows potential for lowering IOP in steroid-induced OHT.
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