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Abstract
Recently, we established silicone oil-induced ocular hypertension (SOHU) mouse model with significant glaucomatous neurodegeneration. Here we characterize two additional variations of this model that simulate two distinct glaucoma types. The first is a chronic model produced by high frequency (HF) pupillary dilation after SO-induced pupillary block, which shows sustained moderate IOP elevation and corresponding slow, mild glaucomatous neurodegeneration. We also demonstrate that although SO removal quickly returns IOP to normal, the glaucomatous neurodegeneration continues to advance to a similar degree as in the HF group without SO removal. The second, an acute model created by no pupillary dilation (ND), shows a greatly elevated IOP and severe inner retina degeneration at an early time point. Therefore, by a straightforward dilation scheme, we extend our original SOHU model to recapitulate phenotypes of two major glaucoma forms, which will be invaluable for selecting neuroprotectants and elucidating their molecular mechanisms.
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Details
1 Stanford University School of Medicine, Department of Ophthalmology, Palo Alto, USA (GRID:grid.168010.e) (ISNI:0000000419368956); Central South University, Department of Ophthalmology, The Second Xiangya Hospital, Changsha, China (GRID:grid.216417.7) (ISNI:0000 0001 0379 7164)
2 Stanford University School of Medicine, Department of Ophthalmology, Palo Alto, USA (GRID:grid.168010.e) (ISNI:0000000419368956); Huazhong University of Science and Technology, Department of Ophthalmology, Union Hospital, Tongji Medical College, Wuhan, China (GRID:grid.33199.31) (ISNI:0000 0004 0368 7223)
3 Stanford University School of Medicine, Department of Ophthalmology, Palo Alto, USA (GRID:grid.168010.e) (ISNI:0000000419368956)