IGF-I及IGF-I受体与视网膜新生血管的研究

本文介绍了IGF-I及IGF-I受体的结构特征、生物功能、及影响因素,以及它们对视网膜新生血管的影响。     

miR-383调控血管生成因子VEGFA的表达并抑制血管生成

目的 探讨miR-383对血管生成的影响及分子机制。 方法 通过生物信息学数据库进行预测,寻找miR-383调控的靶基因,挑选与血管生成相关的靶基因作为候选基因,采用荧光素酶报告基因检测系统进行验证。利用实时荧光定量PCR(qPCR)和Western-blot等实验证实miR-383对候选基因表达的靶向调控; 通过体外血管内皮细胞成管实验检测miR-383对血管生成的影响。 结果 生物信息学预测显示,miR-383靶向多个与血管生成相关的基因; 荧光素酶报告基因实验证实,miR-383可通过结合血管内皮生成因子(VEGFA)基因3''-非翻译区(3''-UTR)而抑制其表达; 过表达miR-383并不影响VEGFA的mRNA转录水平,而只是在蛋白水平下调VEGFA表达; 体外血管生成实验表明,miR-383所介导的VEGFA表达下调可明显抑制血管生成。 结论 miR-383可通过靶向结合VEGFA基因的3''-UTR,抑制其翻译效率而下调VEGFA的表达,并抑制内皮细胞血管生成能力。     

LncRNAs in ocular neovascularizations

The prevalence of eye diseases worldwide is dramatically increasing and represents a major concern in underdeveloped and developed regions. Ocular diseases, previously associated with a higher depression risk, also impose a substantial economic burden on affected families, thus early detection and/or accurate treatment in order to avoid and prevent blindness should be emphasized. Ocular neovascularization (NV), the leading cause of blindness in a variety of eye diseases, is a pathologic process characterized by the formation, proliferation and infiltration of anomalous, tiny and leaky fragile blood vessels within the eye. Genetics have been suspected to play an important role in the occurrence of eye diseases, with the detection of a numbers of specific gene mutations. Long non-coding RNA (lncRNAs) are novel class of regulatory molecules previously associated with various biological processes and diseases, however the nature of the relation and pathways by which they might contribute to the development of corneal, choroidal and retinal NV have not yet been completely elucidated. In this review, we focus on the regulation and characteristics of lncRNAs, summarize results from ocular NV-related studies and discuss the implication of lncRNAs in ocular NV development.     

应用深度增强型成像技术研究早期年龄相关性黄斑变性患者黄斑区脉络膜厚度的变化

目的应用深度增强型相干光断层扫描(EDI-OCT)技术研究早期年龄相关性黄斑变性(AMD)患者黄斑区脉络膜厚度的变化及其与AMD发病的关系。 方法收集2015年3月至2017年3月于中国康复研究中心北京博爱医院眼科就诊的早期AMD患者90例(90只眼)和眼底正常者60例(60只眼)的临床资料。早期AMD患者为患者组,眼底正常者为正常组。患者组中男性51例(51只眼),女性39例(39只眼);年龄63~85岁,平均年龄(74.3±10.9)岁。正常组中男性24例(24只眼),女性36例(36只眼);年龄58~78岁,平均年龄(68.6±10.8)岁。采用EDI-OCT测量两组受试者黄斑中心凹处及由中心凹向鼻侧、颞侧各500 μm、1000 μm处的脉络膜厚度,共测量5个点位。数据以均数±标准差( ±s)表示。两组间脉络膜厚度的比较采用t检验,多组间比较采用单因素方差分析,组间两两比较采用Tukey检验。 结果患者组黄斑区脉络膜的平均厚度为(254.84±51.46)μm;正常组黄斑区脉络膜的平均厚度为(271.46±43.36)μm。患者组黄斑区脉络膜的厚度较正常组低,且两组间差异有统计学意义(t＝-2.061,P<0.05)。所有受试者的年龄与脉络膜的厚度呈负相关,且差异有统计学意义(r＝-0.23,P<0.05)。 结论早期AMD患者的脉络膜厚度较眼底正常者偏薄,且早期AMD患者脉络膜厚度的改变可作为黄斑变性发展的预警因素,能为早期的临床干预提供参考。     

Abrupt visual loss during anti-vascular endothelial growth factor treatment for type 3 neovascularization

AIM: To investigate the incidence of abrupt visual loss and its associated factors, during anti-vascular endothelial growth factor (VEGF) treatment for type 3 neovascularization. METHODS: This retrospective study included 137 eyes that were newly diagnosed with type 3 neovascularization. All eyes were treated with anti-VEGF therapy. Abrupt visual loss was defined as loss of 5 or more lines in best-corrected visual acuity (BCVA) in comparison to the previous visit. The incidence and timing of abrupt visual loss as well as the factors associated with it, were determined. In addition, the BCVA at the final follow-up was compared between the eyes with and those without abrupt visual loss. RESULTS: The mean follow-up period was 42.4±18.9mo after diagnosis, and abrupt visual loss was noted in 22 eyes (16.1%) at a mean of 19.6±13.9mo. Abrupt visual loss was found to be associated with subretinal hemorrhage in 11 eyes (50.0%), development of or increase in the height of pigment epithelial detachment with fluid in 8 eyes (36.4%), and tears in the retinal pigment epithelium in 3 eyes (13.6%). The logarithm of minimum angle of resolution (logMAR) mean BCVA at the final follow-up was 2.07±0.67 (Snellen equivalents: 20/2349) and 1.00±0.55 (20/200) in eyes with and without abrupt visual loss, respectively. BCVA was significantly worse in the eyes with abrupt visual loss (P<0.001). CONCLUSION: Abrupt visual loss is noted in 16.1% of patients with type 3 neovascularization and is associated with poor visual outcome. Additional studies are needed to determine how abrupt visual loss can be prevented.     

角膜塑形镜对近视青少年脉络膜厚度的影响研究

目的随访观察配戴角膜塑形镜及框架眼镜1年的青少年低、中度近视患者,探讨戴镜前后及2组间脉络膜厚度的差异。方法选取-1.00~-6.00 D的252例青少年近视患者,随机分为试验组及对照组,试验组配戴角膜塑形镜,对照组配戴框架眼镜。应用重复测量方差分析、独立样本t检验分析患者治疗1年期间的眼轴,黄斑中心凹及鼻侧、颞侧脉络膜厚度(应用EDI-SD OCT)。结果治疗1年后,试验组患者的眼轴增加明显缓于对照组(低度近视组t=19.071,P<0.001;中度近视组t=19.457,P<0.001);试验组戴镜后各时间点的脉络膜厚度与戴镜前相比均有增厚(P<0.001),低度近视组在戴镜1个月内脉络膜增厚最为明显(P<0.05),1个月后基本趋于稳定(P>0.05),而中度近视组在戴镜3个月内脉络膜增厚最为明显(P<0.05),3个月后基本趋于稳定(P>0.05)。颞侧脉络膜厚度厚于鼻侧。1年后试验组与对照组脉络膜厚度比较差异均有统计学意义(P<0.001)。结论青少年近视患者配戴角膜塑形镜后,眼轴增长变慢,早期脉络膜厚度有不同程度增加,1~3个月后基本保持稳定。     

Efusión uveal asociada a gammapatía monoclonal de significado indeterminado tipo IgM lambda

Case reportA 68-year-old man was referred to the hospital with progressive decreased vision in the right eye over the past year. A moderate cataract and annular choroidal thickening were found. The diagnosis of uveal effusion was confirmed by ultrasound and fluorescein and indocyanine green angiography. Laboratory studies showed an IgM lambda subtype monoclonal gammopathy of undetermined significance. The patient underwent cataract surgery, and a sub-Tenon's triamcinolone injection with a satisfactory short-term outcome.ConclusionThis association has not been previously reported, and it shows that IgM lambda subtype monoclonal gammopathy of undetermined significance should be added to the list of disorders associated with uveal effusion.     

Melatonin attenuated retinal neovascularization and neuroglial dysfunction by inhibition of HIF‐1α‐VEGF pathway in oxygen‐induced retinopathy mice

Retinopathy of prematurity (ROP) is a retinopathy characterized by retinal neovascularization (RNV) occurring in preterm infants treated with high concentrations of oxygen and may lead to blindness in severe cases. Currently, anti‐VEGF therapy is a major treatment for ROP, but it is costly and may cause serious complications. The previous study has demonstrated that melatonin exerted neuroprotective effect against retinal ganglion cell death induced by hypoxia in neonatal rats. However, whether melatonin is anti‐angiogenic and neuroglial protective in the progression of ROP remains unknown. Thus, this study was to investigate the effect of melatonin on RNV and neuroglia in the retina of oxygen‐induced retinopathy (OIR) mice. The results showed a reduction in retinal vascular leakage in OIR mice after melatonin treatment. Besides, the size of retinal neovascular and avascular areas, the number of preretinal neovascular cell nuclei, and the number of proliferative vascular endothelial cells within the neovascular area were significantly decreased in mice treated with melatonin. After oxygen‐induced injury, the density of astrocytes was decreased, accompanied by morphologic and functional changes of astrocytes. Besides, retinal microglia were also activated. Meanwhile, the levels of inflammatory factors were elevated. However, these pathologic processes were all hindered by melatonin treatment. Furthermore, HIF‐1α‐VEGF pathway was activated in the retina of OIR mice, yet was suppressed in melatonin‐treated OIR mice retinas. In conclusion, melatonin prevented pathologic neovascularization, protected neuroglial cells, and exerts anti‐inflammation effect via inhibition of HIF‐1α‐VEGF pathway in OIR retinas, suggesting that melatonin could be a promising therapeutic agent for ROP.