Comparative proteomic analysis of retinal hypoxia-ischemia in an acute ocular hypertension model using tandem mass tag-based quantitative proteomics

IF 3 2区 医学 Q1 OPHTHALMOLOGY Experimental eye research Pub Date : 2024-08-30 DOI:10.1016/j.exer.2024.110063
Guangyi Huang , Lifei Chen , Yunru Lin , Fen Tang , Hui Huang , Qi Chen , Ling Cui , Fan Xu , Chaolan Shen
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Abstract

The main symptom of acute glaucoma is acute ocular hypertension (AOH), which leads to the death of retinal ganglion cells (RGCs) and permanent loss of vision. However, effective treatments for these conditions are lacking. This study aimed to identify major regulators and overall protein changes involved in AOH-induced RGC death. Proteomic patterns of the retinal protein extracts from the AOH and sham groups were analyzed using mass spectrometry (MS), followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.

Proteomic analysis revealed 92 proteins in the AOH group compared to the control group; 58 proteins were upregulated and 34 were downregulated. Alterations in fatty acid-binding protein 7 (FABP7) and caveolin-1 (Cav-1), which are related to fatty acid metabolism and ocular inflammatory signaling, were detected using western blotting and biochemical assays. Variations in the expression of galectin-1 (Gal-1), S100 calcium-binding protein A6 (S100a6), and visinin-like protein-1 (VILIP) have been associated with neuronal ischemia. Our investigation demonstrates that neuroinflammation and fatty acid metabolism are involved in retinal impairment following AOH, suggesting a possible treatment approach for acute glaucoma.

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利用基于串联质量标签的定量蛋白质组学,对急性眼压模型中视网膜缺氧缺血进行比较蛋白质组学分析。
急性青光眼的主要症状是急性眼压升高(AOH),它会导致视网膜神经节细胞(RGC)死亡,并造成永久性视力丧失。然而,目前还缺乏针对这些症状的有效治疗方法。本研究旨在确定AOH诱导RGC死亡所涉及的主要调节因子和整体蛋白质变化。研究人员使用质谱(MS)分析了AOH组和假视网膜组视网膜蛋白质提取物的蛋白质组学模式,然后进行了基因本体(GO)和京都基因与基因组百科全书(KEGG)通路分析。蛋白质组分析显示,与对照组相比,AOH 组有 92 个蛋白质上调,其中 58 个上调,34 个下调。利用Western印迹和生化分析检测到了脂肪酸结合蛋白7(FABP7)和洞穴素-1(Cav-1)的变化,这两种蛋白与脂肪酸代谢和眼部炎症信号转导有关。galectin-1(Gal-1)、S100钙结合蛋白A6(S100a6)和粘蛋白样蛋白-1(VILIP)的表达变化与神经元缺血有关。我们的研究表明,神经炎症和脂肪酸代谢参与了 AOH 引起的视网膜损伤,这为急性青光眼的治疗提供了一种可能的方法。
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来源期刊
Experimental eye research
Experimental eye research 医学-眼科学
CiteScore
6.80
自引率
5.90%
发文量
323
审稿时长
66 days
期刊介绍: The primary goal of Experimental Eye Research is to publish original research papers on all aspects of experimental biology of the eye and ocular tissues that seek to define the mechanisms of normal function and/or disease. Studies of ocular tissues that encompass the disciplines of cell biology, developmental biology, genetics, molecular biology, physiology, biochemistry, biophysics, immunology or microbiology are most welcomed. Manuscripts that are purely clinical or in a surgical area of ophthalmology are not appropriate for submission to Experimental Eye Research and if received will be returned without review.
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