Peng Michael, Curry Stacy M, Liu Yang, Lohawala Husain, Sharma Gaurav, Sharma Tasneem P
Eugene and Marilyn Glick Eye Institute, Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
North Texas Eye Research Institute, Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA.
NPJ Microgravity. 2022 Oct 28;8(1):44. doi: 10.1038/s41526-022-00232-5.
Spaceflight-Associated Neuro-ocular Syndrome (SANS) is a significant unexplained adverse reaction to long-duration spaceflight. We employ an ex vivo translaminar autonomous system (TAS) to recreate a human ocular ground-based spaceflight analogue model to study SANS pathogenesis. To recapitulate the human SANS conditions, human ocular posterior segments are cultured in the TAS model for 14 days. Translaminar pressure differentials are generated by simulating various flow rates within intracranial pressure (ICP) and intraocular (IOP) chambers to maintain hydrostatic pressures of ICP: IOP (12:16, 15:16, 12:21, 21:16 mmHg). In addition, optic nerves are mechanically kinked by 6- and 10-degree tilt inserts for the ICP: IOP;15:16 mmHg pressure paradigm. The TAS model successfully maintains various pressure differentials for all experimental groups over 14 days. Post culture, we determine inflammatory and extracellular component expression changes within posterior segments. To further characterize the SANS pathogenesis, axonal transport capacity, optic nerve degeneration and retinal functional are measured. Identifiable pathogenic alterations are observed in posterior segments by morphologic, apoptotic, and inflammatory changes including transport and functional deficits under various simulated SANS conditions. Here we report our TAS model provides a unique preclinical application system to mimic SANS pathology and a viable therapeutic testing device for countermeasures.
航天相关神经眼综合征(SANS)是长期太空飞行中一种重大的不明原因不良反应。我们采用体外跨层自主系统(TAS)来重建一个基于地面的人类眼部太空飞行模拟模型,以研究SANS的发病机制。为了重现人类SANS情况,将人类眼后段在TAS模型中培养14天。通过模拟颅内压(ICP)和眼内压(IOP)腔内的各种流速来产生跨层压力差,以维持ICP:IOP的静水压力(12:16、15:16、12:21、21:16 mmHg)。此外,对于ICP:IOP为15:16 mmHg的压力模式,通过6度和10度倾斜插入物对视神经进行机械扭结。TAS模型在14天内成功为所有实验组维持了各种压力差。培养后,我们确定眼后段内炎症和细胞外成分表达的变化。为了进一步表征SANS的发病机制,测量轴突运输能力、视神经变性和视网膜功能。在各种模拟的SANS条件下,通过形态学、凋亡和炎症变化,包括运输和功能缺陷,在眼后段观察到可识别的致病改变。在此我们报告,我们的TAS模型提供了一个独特的临床前应用系统来模拟SANS病理学,以及一个可行的对策治疗测试装置。