Transcriptional responses in a mouse model of silicone wire embolization induced acute retinal artery ischemia and reperfusion

作者：Yuedan Wang, Ying Li, Jiaqing Feng, Chuansen Wang, Yuwei Wan, Bingyang Lv, Yin‐Ming Li, Hao Xie, Ting Chen, Faxi Wang, Ziyue Li, Anhuai Yang, Xuan Xiao · 发表于：eLife · 年份：2024 · DOI：10.7554/elife.98949 · 被引用次数：4 · 研究领域：Retinal and Optic Conditions、Neuroinflammation and Neurodegeneration Mechanisms、Ocular Diseases and Behçet’s Syndrome

Acute retinal ischemia and ischemia-reperfusion injury are the primary causes of retinal neural cell death and vision loss in retinal artery occlusion (RAO). The absence of an accurate mouse model for simulating the retinal ischemic process has hindered progress in developing neuroprotective agents for RAO. We developed a unilateral pterygopalatine ophthalmic artery occlusion (UPOAO) mouse model using silicone wire embolization combined with carotid artery ligation. The survival of retinal ganglion cells and visual function were evaluated to determine the duration of ischemia. Immunofluorescence staining, optical coherence tomography, and haematoxylin and eosin staining were utilized to assess changes in major neural cell classes and retinal structure degeneration at two reperfusion durations. Transcriptomics was employed to investigate alterations in the pathological process of UPOAO following ischemia and reperfusion, highlighting transcriptomic differences between UPOAO and other retinal ischemia-reperfusion models. The UPOAO model successfully replicated the acute interruption of retinal blood supply observed in RAO. 60 min of Ischemia led to significant loss of major retinal neural cells and visual function impairment. Notable thinning of the inner retinal layer, especially the ganglion cell layer, was evident post-UPOAO. Temporal transcriptome analysis revealed various pathophysiological processes related to immune cell migration, oxidative stress, and immune inflammati...