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Updated: Jan 8, 2026

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A Laser-induced Mouse Model of Chronic Ocular Hypertension to Characterize Visual Defects
Published on: August 14, 2013
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Mechanistic Insights into Glucocorticoid-Induced Ocular Hypertension Using Differences in Mouse Strain Responsiveness
Pinkal D Patel1, Gaurang C Patel2, J Cameron Millar1
1Pharmacology and Neuroscience, North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, Texas.
The American Journal of Pathology
|December 17, 2025
Summary
Glucocorticoid therapy can cause ocular hypertension. Researchers identified specific mouse strains susceptible to this side effect, revealing potential biomarkers and mechanisms for GC-induced ocular hypertension and related glaucomas.
Area of Science:
- Ophthalmology
- Pharmacology
- Genetics
Background:
- Glucocorticoids (GCs) are common anti-inflammatory drugs.
- Long-term GC use can cause GC-induced ocular hypertension (GC-OHT), a precursor to secondary glaucoma, affecting ~40% of patients.
- The molecular mechanisms of GC-OHT remain poorly understood.
Purpose of the Study:
- To identify biomarkers for GC susceptibility.
- To elucidate the molecular mechanisms underlying GC-OHT.
- To compare phenotypic and transcriptomic differences in GC-OHT development across mouse strains.
Main Methods:
- Developed a mouse model of GC-OHT using dexamethasone.
- Compared phenotypic and transcriptomic data from five genetically distinct inbred mouse strains.
- Analyzed intraocular pressure (IOP) and trabecular meshwork gene expression.
Main Results:
- Mouse strains exhibited varied susceptibility to GC-OHT, mirroring human responses.
- C57BL/6J and C3H/HeJ mice were identified as GC responders with higher IOP after dexamethasone treatment.
- Transcriptomic analysis revealed novel trabecular meshwork biomarkers associated with GC-OHT susceptibility.
Conclusions:
- Genetic background significantly influences GC-OHT development.
- Identified potential molecular pathways and biomarkers for GC-OHT.
- Findings offer insights into GC-OHT pathogenesis and primary open-angle glaucoma.

