Department of Ophthalmology, Kağızman State Hospital, Kars, Turkey.
Department of Ophthalmology, Atatürk Training and Research Hospital, Ankara, Turkey.
Mol Biol Rep. 2020 Dec;47(12):9337-9344. doi: 10.1007/s11033-020-05994-3. Epub 2020 Nov 16.
Analysis of the reactive oxygen species (ROS)-detoxifying biomarkers may elucidate the mitochondrial dysfunction in glaucoma pathogenesis. Therefore, we purposed to investigate the effects of ROS-detoxifying molecules including Silent Information Regulator T1 (SIRT1) and Forkhead Box O 1 (FOXO1) and 3a (FOXO3a) transcription factors in patients with glaucoma. Our analyses included 20 eyes from patients with primary open-angle glaucoma (POAG) and 20 eyes from patients with pseudoexfoliation glaucoma (PXG) who were scheduled for trabeculectomy. After extraction of total RNA from trabecular meshwork tissue, we compared the levels of SIRT1, FOXO1and FOXO3a genes in the oxidative pathway with the level of glyceraldehyde-3 phosphate dehydrogenase (GAPDH), the reference gene, using real-time polymerase chain reaction. Relative gene expression was calculated using the threshold cycle (2) method. We observed similarly reduced expression levels of SIRT1, FOXO1, and FOXO3a genes versus GAPDH among patient groups (p = 0.40; p = 0.56; p = 0.35, respectively). This is the first study to identify the role of SIRT1 and FOXOs in human TM with glaucoma. Relative expression levels of SIRT1, FOXO1, and FOXO3a genes versus a control gene (GAPDH) were decreased in POAG and PXG groups. Our results show that SIRT1and FOXOs (1-3a) deserve special attention in the pathogenesis of glaucoma.
活性氧(ROS)解毒生物标志物的分析可能阐明青光眼发病机制中的线粒体功能障碍。因此,我们旨在研究包括沉默信息调节因子 T1(SIRT1)和叉头框 O 1(FOXO1)和 3a(FOXO3a)转录因子在内的 ROS 解毒分子对青光眼患者的影响。我们的分析包括 20 例原发性开角型青光眼(POAG)和 20 例拟行小梁切除术的假性剥脱性青光眼(PXG)患者的 20 只眼。从小梁网组织中提取总 RNA 后,我们使用实时聚合酶链反应比较了氧化途径中 SIRT1、FOXO1 和 FOXO3a 基因与甘油醛-3-磷酸脱氢酶(GAPDH)(参考基因)的水平。使用阈值循环(2)法计算相对基因表达。我们观察到患者组中 SIRT1、FOXO1 和 FOXO3a 基因相对于 GAPDH 的表达水平相似降低(p=0.40;p=0.56;p=0.35,分别)。这是第一项确定 SIRT1 和 FOXOs 在人类 TM 与青光眼中的作用的研究。POAG 和 PXG 组中 SIRT1、FOXO1 和 FOXO3a 基因相对于对照基因(GAPDH)的相对表达水平降低。我们的结果表明,SIRT1 和 FOXOs(1-3a)在青光眼发病机制中值得特别关注。