AI Article Synopsis
- Extended glucocorticoid treatment can cause ocular hypertension and lead to iatrogenic open-angle glaucoma, resembling primary open-angle glaucoma (POAG).
- Researchers have shown that weekly injections of dexamethasone-21-acetate in mice result in significant intraocular pressure (IOP) increase, retinal ganglion cell loss, and optic nerve damage.
- The mouse model exhibits key features of POAG and can be used to explore how glaucoma affects the trabecular meshwork and retinal ganglion cell axons, as well as to test new treatment methods.
Article Abstract
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.
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| http://dx.doi.org/10.1007/978-1-0716-4140-8_12 | DOI Listing |
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