Mouse Model of Glucocorticoid-Induced Glaucoma.

Autor:	Maddineni P; Gavin Herbert Eye Institute-Center for Translational Vision Research, Department of Ophthalmology, Department of Physiology and Biophysics, University of California Irvine School of Medicine, Irvine, California, USA.; Department of Ophthalmology, School of Medicine, University of Missouri, Columbia, USA., Sundaresan Y; Gavin Herbert Eye Institute-Center for Translational Vision Research, Department of Ophthalmology, Department of Physiology and Biophysics, University of California Irvine School of Medicine, Irvine, California, USA., Zode G; Gavin Herbert Eye Institute-Center for Translational Vision Research, Department of Ophthalmology, Department of Physiology and Biophysics, University of California Irvine School of Medicine, Irvine, California, USA. gzode@uci.edu.
Jazyk:	angličtina
Zdroj:	Methods in molecular biology (Clifton, N.J.) [Methods Mol Biol] 2025; Vol. 2858, pp. 131-141.
DOI:	10.1007/978-1-0716-4140-8_12
Abstrakt:	Extended glucocorticoid (GC) treatment can lead to ocular hypertension and induce iatrogenic open-angle glaucoma. GC-induced glaucoma mimics many clinical and pathological features of primary open-angle glaucoma (POAG), and therefore mouse models of GC-induced glaucoma are utilized to study pathophysiology of glaucoma. We have recently demonstrated that weekly periocular injections of dexamethasone-21-acetate (Dex-Ac) lead to robust and significant intraocular pressure (IOP) elevation, retinal ganglion cell (RGC) loss, and optic nerve degeneration in mice. Our mouse model exhibits signature features of POAG including significant IOP elevation due to reduced outflow facility, progressive optic nerve degeneration, and structural and functional loss of RGCs. Dex-induced IOP elevation is associated with increased aqueous outflow resistance due to trabecular meshwork (TM) dysfunction including excessive extracellular matrix deposition and induction of endoplasmic reticulum stress. Mouse model of Dex-induced glaucoma represents an ideal animal model to investigate both glaucomatous damage to the TM and RGC axons and to develop novel therapies. Here, we present a detailed protocol for developing this model in laboratory settings. (© 2025. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze:	MEDLINE
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