Department of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA, 94304, USA.
Department of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Sci Rep. 2021 Apr 27;11(1):9052. doi: 10.1038/s41598-021-88690-x.
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.
最近，我们建立了一种硅酮油诱导的眼高压（SOHU）小鼠模型，该模型具有明显的青光眼神经退行性变。在这里，我们描述了该模型的另外两种变化，它们模拟了两种不同的青光眼类型。第一种是通过 SOH 引起的瞳孔阻滞后的高频（HF）瞳孔扩张产生的慢性模型，该模型显示持续的中度 IOP 升高和相应的缓慢、轻度青光眼神经退行性变。我们还证明，尽管 SO 去除后眼压迅速恢复正常，但青光眼神经退行性变仍会继续进展，其程度与不进行 SO 去除的 HF 组相似。第二种是通过不扩张瞳孔（ND）产生的急性模型，在早期表现出极高的眼压和严重的内视网膜变性。因此，通过一种简单的扩张方案，我们将原始的 SOHU 模型扩展到了两种主要青光眼形式的表型重现，这对于选择神经保护剂和阐明其分子机制将是非常宝贵的。
