Background: Long non-coding RNA homeobox A11 antisense RNA (HOXA11-AS) has been reported to be involved in initiation and development of multiple cancers. However, the detailed biological roles and underlying molecular mechanism of HOXA11-AS remain unclear in retinoblastoma (RB). Herein, the goals of this study were to explore the biological function and the potential mechanism of HOXA11-AS in RB. Materials and methods: The expression of HOXA11-AS in RB tissues and cell lines was detected using real-time PCR (qRT-PCR). Cell proliferation, cycle arrest and apoptosis were measured using a cell counting kit 8 and flow cytometry. The target miRNAs of HOXA11-AS was predicted by Starbase2.0 software and was confirmed using a dual-luciferase reporter assay. Result: We found that HOXA11-AS expression was markedly elevated in RB tissues and cell lines compared to normal retina tissues and human retinal epithelial cells, respectively. Functional analysis showed that knockdown of HOXA11-AS in RB cells significantly suppressed cell proliferation, and induced cell cycle arrest at G1/G0 phase and promoted cell apoptosis. We also found that HOXA11-AS could serve as a competing endogenous RNA (ceRNA) that inhibited miR-506-3p expression, which regulated its downstream target NIMA-related kinase 6 (NEK6) in RB. In addition, miR-506-3p inhibitors partially reversed the effect of HOXA11-AS depletion on proliferation, cycle arrest and apoptosis in RB cells. Conclusion: Taken together, these findings demonstrated that HOXA11-AS could promote RB progression by sponging miR-506-3p, suggesting that HOXA-11-AS might be a potential therapeutic target for RB.

To study the alteration of cytokine factors in aqueous humor and retinal microstructure in the formation of serous retinal detachment (SRD) secondary to retinal vein occlusion. The subjects were 39 patients with RVO, of whom 31 patients had SRD (RVO-SRD). Spectral Domain Optical Coherence Tomography (SD-OCT) was used to measure the completeness of photoreceptor inner segment/outer segment (IS/OS) and the external limiting membrane (ELM) as well as the structure of RVO-SRD, including the height and shape of SRD. The aqueous humor was collected before intravitreal injection of Ranibizumab. The concentrations of VEGF, MCP-1, IL-8, IL-6, b-FGF and TNF-α in the aqueous humor were measured. All patients participated in the 6-month follow-up examinations, which included visual acuity, intraocular pressure, ophthalmologic examination, and SD-OCT. The time of recurrence of RVO-SRD was recorded. The formation of SRD was associated with the area of congested vein, disrupted IS/OS, ELM layers and high VEGF, MCP-1, IL-8, IL-6 levels. However, the height and shape of SRD were not relevant to any inflammatory factors. Moreover, high levels of MCP-1, IL-8 and IL-6 were found in large areas of congested veins. High levels of MCP-1 and IL-6 were observed in the patients with incomplete IS/OS and ELM. The recurrence of SRD was related to the high MCP-1 level. High concentrations of cytokine factors in aqueous humor could induce vascular leakage, exacerbate the extent of macular edema, disrupt the structure of ELM and IS/OS, and develop SRD in RVO.

Introduction: Terson's syndrome with inner limiting membrane (ILM) peeled off spontaneously is rarely seen, and the mechanism of it is not clear. Here we report a case of Terson Syndrome with a rare finding: the ILM peeled off spontaneously associated with macular hole (MH). Patient concerns: A 36-year-old female patient was admitted to our hospital with decreased visual acuity in the right eye lasting for 1 month. She just had surgery for subarachnoid hemorrhage that occurred 1 month before due to the rupture of the intracranial aneurysm. Diagnosis: Terson syndrome was diagnosed according to her medical history and examination. A partial posterior vitreous detachment (PVD) and dense vitreous hemorrhage (VH) was confirmed in the right eye by performing ophthalmic B-scan ultrasonography examination. Head computed tomography showed the subarachnoid hemorrhage after aneurysmal rupture. Interventions: The patient underwent pars plana vitrectomy in her right eye to remove the VH. After removal of the VH, a full-thickness macular hole was noted with the ILM peeled off spontaneously. So we conducted gas tamponade, and face-down positioning after pas plana vitrectomy. Outcomes: At two weeks follow-up, her best corrected visual acuity was 0.15 in the right eye. Spectral domain optical coherence tomography showed that the MH was closed completely, while the thickness of the nasal retina of the foveal was thicker than that on the temporal side. Lessons: ILM peeled off spontaneously associated with MH is a rarely seen complication of Terson Syndrome. Due to the large-scale of the ILM peeling off, final visual acuity may be poor in patients, even though successful macular hole closure after the operation.

Introduction: One of the most common vascular diseases of the retina is diabetic retinopathy (DR), a microvascular condition caused by diabetes. The autophagy system transports and degrades cytoplasmic substances to lysosomes as part of the intracellular degradation process. Autophagy appears to be an important regulator in the development and progression of DR, but its mechanism and potential role are unclear. The purpose of this study is to identify autophagy-related genes in DR and find potential biomarkers associated with DR through bioinformatics analysis.Method: We retrieved the dataset GSE102485 from the Gene Expression Omnibus (GEO) database and compiled a list of 344 autophagy-related genes. Using the R software, bioinformatics analysis was used to identify the differentially expressed autophagy-related genes (ARGs). Then, we identified the autophagy-related hub genes (ARHGs) through a series of analyses including Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, correlation analysis, and protein-protein interaction (PPI) network. In addition, the miRNA-gene-TF interaction network was generated using the NetworkAnalyst platform. Potential therapeutic drugs were predicted utilizing the Drug-Gene Interaction Database (DGIdb). Ultimately, DR was simulated through the high glucose incubation of the retinal pigment epithelium cell line (ARPE-19), and employing quantitative real-time polymerase chain reaction (qRT-PCR) to verify ARHG expression. The effectiveness of ARHGs in diagnosing DR was assessed by measuring the area under the receiver operating characteristic (ROC) curve.Results: Differential expression analysis identified 26 ARGs, of which 6 were upregulated and 20 were downregulated. Through GO and KEGG enrichment analysis, it was found that ARGs showed significant enrichment in autophagy-related pathways. Using PPI network analysis, 7 ARHGs were identified. The expression of MAPK8, HDAC6, DNAJB1 and TARDBP, in a model of DR were confirmed by qRT-PCR. The ROC curve results showed that MAPK8, HDAC6, DNAJB1 and TSC2 had high predictive accuracy and could be used as biomarkers for DR.Conclusion: Through bioinformatics analysis, we identified 26 genes that may be associated with autophagy in DR. We suggest that the hub genes MAPK8 and HDAC6 as biomarkers may be involved in autophagy in DR.

Purpose The purpose of this study is to investigate the role of Secretogranin III (Scg3) in the pathogenesis of intraocular neovascular diseases and assess its potential as a therapeutic target for novel treatment strategies. Methods A literature review was conducted to examine the expression of Scg3 in intraocular neovascular diseases. We reviewed studies on the interaction of Scg3 with its homologous receptors and its effect on endothelial cell proliferation, migration, and vascular permeability—key processes involved in angiogenesis and neovascularization. Results Scg3 was found to be upregulated in the tissues affected by diabetic retinopathy (DR), retinopathy of prematurity (ROP), and choroidal neovascularization. In DR, Scg3 expression was linked to retinal neovascularization, where it facilitated endothelial cell proliferation and migration, essential processes for the formation of new blood vessels. Similarly, in ROP, Scg3 was associated with fibrovascular tissue proliferation within avascular retinal zones, contributing to the pathological neovascularization seen in premature infants. In the context of age-related macular degeneration (AMD), Scg3 appeared to play a role in choroidal neovascularization, where it promoted the invasion of choroidal capillaries into the retinal pigment epithelium. Furthermore, Scg3’s binding to its homologous receptors was shown to enhance vascular permeability, potentially exacerbating fluid leakage and edema in these diseases, which is a hallmark of exudative conditions. Collectively, these findings suggest that Scg3 plays a pivotal role in driving angiogenesis and vascular permeability in intraocular neovascular diseases Conclusion The upregulation of Scg3 in DR, ROP, and choroidal neovascularization highlights its potential as a novel therapeutic target. Inhibition of Scg3 could offer a new avenue for treating these sight-threatening conditions.