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Abstract：
Primary open-angle glaucoma (POAG) is subdivided depending on eye pressure. Patients with normal-tension glaucoma (NTG) have never had high intraocular pressure (IOP) measured while patients with ocular hypertension (OHT) have high eye pressure but no signs of glaucoma. Although IOP is considered to be a risk factor for all glaucoma patients, it is reasonable to assume that other risk factors such as inflammation play a role. We aimed to characterize the proteome and cytokine profile during hypoxia in plasma from patients with NTG (n = 10), OHT (n = 10), and controls (n = 10). Participants were exposed to hypoxia for two hours, followed by 30 min of normoxia. Samples were taken before (\"baseline\"), during (\"hypoxia\"), and after hypoxia (\"recovery\"). Proteomics based on liquid chromatography coupled with mass spectrometry (LC-MS) was performed. Cytokines were measured by Luminex assays. Bioinformatic analyses indicated the involvement of complement and coagulation cascades in NTG and OHT. Regulation of high-density lipoprotein 3 (HDL3) apolipoproteins suggested that changes in cholesterol metabolism are related to OHT. Hypoxia decreased the level of tumor necrosis factor-α (TNF-α) in OHT patients compared to controls. Circulating levels of interleukin-1β (IL-1β) and C-reactive protein (CRP) were decreased in NTG patients compared to controls during hypoxia. After recovery, plasma interleukin-6 (IL-6) was upregulated in patients with NTG and OHT. Current results indicate an enhanced systemic immune response in patients with NTG and OHT, which correlates with pathogenic events in glaucoma. Apolipoproteins may have anti-inflammatory effects, enabling OHT patients to withstand inflammation and development of glaucoma despite high IOP.
摘要：
原发性开角型青光眼（POAG）根据眼压细分。正常眼压青光眼（NTG）患者从未测量过高眼压（IOP），而高眼压（OHT）患者眼压高，但没有青光眼迹象。虽然IOP被认为是所有青光眼患者的危险因素，可以合理地假设炎症等其他危险因素也起作用。我们旨在表征NTG患者血浆缺氧期间的蛋白质组和细胞因子谱（n=10），OHT（n=10），和控制（n=10）。参与者暴露于缺氧两个小时，然后是30分钟的常氧。之前取样(“基线”)，在(“缺氧”)期间，和缺氧后（“恢复”）。进行基于液相色谱与质谱联用(LC-MS)的蛋白质组学。通过Luminex测定法测量细胞因子。生物信息学分析表明补体和凝血级联参与NTG和OHT。高密度脂蛋白3（HDL3）载脂蛋白的调节表明，胆固醇代谢的变化与OHT有关。与对照组相比，缺氧降低了OHT患者的肿瘤坏死因子-α（TNF-α）水平。与对照组相比，缺氧期间NTG患者的白细胞介素-1β（IL-1β）和C反应蛋白（CRP）的循环水平降低。恢复后,NTG和OHT患者血浆白细胞介素-6（IL-6）上调。目前的结果表明，NTG和OHT患者的全身免疫反应增强，这与青光眼的致病事件有关。载脂蛋白可能具有抗炎作用，使OHT患者能够承受炎症和青光眼的发展，尽管高IOP。
