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Elife. 2019 May 15;8. pii: e45881. doi: 10.7554/eLife.45881.

Silicone oil-induced ocular hypertension and glaucomatous neurodegeneration in mouse.

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Department of Ophthalmology, Stanford University School of Medicine, Palo Alto, United States.
Department of Ophthalmology, Tongji Medical College, Union Hospital, Huazhong University of Science & Technology, Wuhan, China.
Department of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, China.
Department of Ophthalmology, Veterans Affairs Palo Alto Health Care, Palo Alto, United States.
Contributed equally


Understanding the molecular mechanism of glaucoma and development of neuroprotectants is significantly hindered by the lack of a reliable animal model that accurately recapitulates human glaucoma. Here, we sought to develop a mouse model for the secondary glaucoma that is often observed in humans after silicone oil (SO) blocks the pupil or migrates into the anterior chamber following vitreoretinal surgery. We observed significant intraocular pressure (IOP) elevation after intracameral injection of SO, and that SO removal allows IOP to return quickly to normal. This simple, inducible and reversible mouse ocular hypertension model shows dynamic changes of visual function that correlate with progressive retinal ganglion cell (RGC) loss and axon degeneration. It may be applicable with only minor modifications to a range of animal species in which it will generate stable, robust IOP elevation and significant neurodegeneration that will facilitate selection of neuroprotectants and investigating the pathogenesis of ocular hypertension-induced glaucoma.


glaucoma; intraocular pressure; mouse; neurodegeneration; neuroprotection; neuroscience; optic nerve; retinal ganglion cell

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