Abstract：
Rhegmatogenous retinal detachment (RRD) is a type of ophthalmologic emergency, if left untreated, the blindness rate approaches 100 %. The RRD patient postoperative recovery of visual function is unsatisfactory, most notably due to photoreceptor death. We conducted to identify the key genes for oxidative stress (OS) in RRD through bioinformatics analysis and clinical validation, thus providing new ideas for the recovery of visual function in RRD patients after surgery. A gene database for RRD was obtained from the Gene Expression Omnibus (GEO) database (GSE28133). Then we screened differentially expressed OS genes (DEOSGs) from the database and assessed the critical pathways in RRD with Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Protein-protein interaction (PPI) networks and hub genes among the common DEOSGs were identified. In addition, we collected general information and vitreous fluid from 42 patients with RRD and 22 controls [11 each of epiretinal membrane (EM) and macular hole (MH)], examined the expression levels of proteins encoded by hub genes in vitreous fluid by enzyme-linked immunosorbent assay (ELISA) to further assess the relationship between the ELISA data and the clinical characteristics of patients with RRD. Ten hub genes (CCL2, ICAM1, STAT3, CD4, ITGAM, PTPRC, CCL5, IL18, TLR2, VCAM1) were finally screened out from the dataset. The ELISA results showed that, compared with the control group, patients with RRD: TLR2 and ICAM-1 were significantly elevated, and CCL2 had a tendency to be elevated, but no statistically significant; RRD patients and MH patients compared with EM patients: STAT3 and VCAM-1 were significantly elevated. We found affected eyes of RRD patients compared with healthy eyes: temporal and nasal retinal nerve fiber layer (RNFL) were significantly thickened. By correlation analysis, we found that: STAT3 was negatively correlated with ocular perfusion pressure (OPP); temporal RNFL was not only significantly positively correlated with CCL2, but also negatively correlated with Scotopic b-wave amplitude. These findings help us to further explore the mechanism of RRD development and provide new ideas for finding postoperative visual function recovery.
摘要：
孔源性视网膜脱离（RRD）是一种眼科急症，如果不及时治疗，失明率接近100%。RRD患者术后视功能恢复不理想，最值得注意的是由于光感受器死亡。我们通过生物信息学分析和临床验证来鉴定RRD中氧化应激（OS）的关键基因，从而为RRD患者术后视功能的恢复提供新思路。从基因表达综合(GEO)数据库(GSE28133)获得RRD的基因数据库。然后，我们从数据库中筛选了差异表达的OS基因（DEOSGs），并通过基因本体论（GO）和京都基因和基因组百科全书（KEGG）途径评估了RRD中的关键途径。鉴定了常见DEOSGs之间的蛋白质-蛋白质相互作用（PPI）网络和hub基因。此外,我们收集了42例RRD患者和22例对照[11例视网膜前膜（EM）和黄斑裂孔（MH）]的一般信息和玻璃体液，通过酶联免疫吸附试验（ELISA）检查玻璃体液中hub基因编码的蛋白质的表达水平，以进一步评估ELISA数据与RRD患者临床特征之间的关系。十个hub基因(CCL2、ICAM1、STAT3、CD4、ITGAM、PTPRC,最后从数据集中筛选出CCL5、IL18、TLR2、VCAM1)。ELISA结果显示,与对照组相比，RRD患者：TLR2和ICAM-1显著升高，CCL2有升高的趋势，但无统计学意义；RRD患者和MH患者与EM患者相比：STAT3和VCAM-1均显著升高。我们发现RRD患者的受影响眼睛与健康眼睛相比：颞部和鼻腔视网膜神经纤维层（RNFL）显着增厚。通过相关性分析，我们发现：STAT3与眼灌注压（OPP）呈负相关；时间RNFL不仅与CCL2呈显着正相关，而且与Scotopicb波振幅呈负相关。这些发现有助于我们进一步探讨RRD发生发展的机制,为发现术后视功能恢复提供新思路。
