微小核糖核酸与眼底疾病的相关性研究进展

微小核糖核酸(miRNA)是近年来发现的真核细胞内一类稳定、非编码可调控的核糖核酸(RNA)分子,主要通过与靶基因信使RNA(mRNA)3’端非编码区碱基配对的方式,引起靶标mRNA降解或翻译抑制,从而参与真核生物的生长发育、细胞增生凋亡及肿瘤发生等多种生理和病理过程.miRNA表达变化与眼底新生血管性疾病、糖尿病视网膜病变、视网膜色素变性、视网膜母细胞瘤、脉络膜黑色素瘤等眼底疾病的发生发展存在一定的相关性.进一步探索miRNA与眼底疾病发生发展的相互关系,可能有助于从基因水平上认识、预防和治疗这些眼底疾病.     

细胞外囊泡miRNA在糖尿病视网膜病变发病机制中的作用

细胞外囊泡是包含微囊泡、外泌体和凋亡小体的纳米级囊泡,外泌体包含蛋白质、脂质和微小RNA(miRNAs)等内容物。miRNAs是一类高度保守、非编码的小分子RNA,通过与靶基因转录的mRNA互补配对在转录后水平调节靶基因的表达,可在广泛生物细胞分泌的细胞外囊泡中存在。近年来发现miRNAs与糖尿病视网膜病变的发生发展密切相关,是糖尿病视网膜病变的早期检测和治疗的生物标志物。本文就部分miRNAs(miR-126、miR-29b、miR-200b、miR-1273G-3p、miR-93、miR-142-5p)在视网膜的表达以及对其靶基因在糖尿病视网膜病变发病机制中的作用进行综述。     

miRNA在新生血管性眼病中作用的研究进展

微小RNA( miRNAs)是一类高度保守、非编码的小分子RNA,通过与靶基因转录的mRNA互补配对在转录后水平调节靶基因的表达,人类约有1/3的基因受miRNAs调控.新生血管性眼病是眼科的难治性疾病和重要的致盲原因.最新研究表明,miRNAs在眼内新生血管的发生发展中起到十分重要的调控作用.miRNAs用于治疗新生血管性眼病具有广阔的前景.就miRNAs的功能及其在眼部的表达、miRNAs与眼内新生血管及血管生成因子的关系、miRNAs在糖尿病视网膜病变中的研究现状进行综述.     

MicroRNAs在晶状体中的功能

MicroRNAs(miRNAs)是一类包含21～23个碱基的非编码单链小分子RNA。通过与靶基因3'端非翻译区(UTR)不完全碱基配对,使mRNA降解或抑制靶mRNA的翻译,进而发挥基因调控作用。miRNAs广泛参与生物体内的多种生理和病理过程,通过其表达量的上调或下调,影响细胞发育和疾病的进程。近年来许多研究表明,miRNAs在眼部的多种组织,包括晶状体、视网膜和角膜中均有表达,其异常表达可能与某些眼部疾病的发生、发展有密切关系。本文综述近年来miRNAs在晶状体中的表达、功能及研究进展,以期寻求可用于临床诊断、治疗晶状体混浊的新型靶点。     

MicroRNAs在糖尿病视网膜病变中的相关研究进展

MicroRNAs(miRNAs)是一种小分子非编码RNA,是转录后调节基因表达关键因子,参与调控细胞分化、增殖和新陈代谢等多种生物学过程。在糖尿病视网膜病变(DR)发生发展过程中miRNAs表达差异改变明显,国内外多项研究表明miRNAs调控基因的表达与DR生理病理机制关系密切。部分特异性表达的miRNAs可以通过调控视网膜中氧化应激与炎症反应水平等影响DR发生发展,因此通过增强或抑制这部分miRNAs可以延缓DR病情进展。单个或多个miRNAs的组合可以作为DR新型的转录组学生物标志物,也是未来治疗DR的潜在有效靶点。目前针对血液或体液中特定miRNAs的检测有助于DR的早期干预治疗和病情随访追踪。因此,本文主要对miRNAs及其参与调控DR的分子机制、治疗前景及生物标志物的相关研究进展作一综述。     

微小RNA在视网膜中的表达及其与视网膜疾病的关系

微小RNA(microRNA.miRNAs)是一类调控基因表达的非编码小RNA.miRNA的表达具有组织特异性,并参与细胞生长、发育、分化、增生以及凋亡等过程.近年来,人们也发现miRNA在视网膜不同细胞中呈特异表达,尽管尚无直接证据,但这些差异表达的miRNA可能与视网膜疾病如视网膜色素变性以及糖尿病视网膜病变的发生发展有着密切的联系.本文对miRNA在视网膜中的特异表达以及miRNA在视网膜疾病中的作用等研究现状进行总结,同时对miRNA在视网膜相关疾病的治疗方面的前景进行探讨.     

哺乳动物视网膜microRNA的表达及功能

microRNAs(miRNAs)是一类长约22个核苷酸的内源性非编码单链RNA,在维系几乎所有组织或器官系统的正常发育和生理功能等方面都起着非常重要的作用,主要通过降解靶基因mRNAs或抑制靶基因mRNAs的翻译,从而沉默特定靶基因发挥作用.据预测人类超过1/3的蛋白编码基因受miRNAs的调控.越来越多的研究表明很多miRNAs在眼部组织中有特异性的表达,其中至少有78个miRNAs在视网膜组织中表达.本文主要就miRNAs在哺乳动物视网膜中的表达及其相关功能的最新研究进展作一综述.     

微小RNA在糖尿病视网膜病变发病机制中的作用

微小RNA（micoRNA）是一类高度保守、非编码的小分子RNA,通过与mRNA互补配对在转录后水平降解mRNA或抑制mRNA翻译来负调控靶基因的表达,并可能调控着几乎每一个细胞生理进程.研究发现微小RNA的异常表达谱对于糖尿病视网膜病变（diabetic retinopathy,DR）的发病机制有着至关重要的作用.微小RNA在不同的刺激因素下通过靶向调控核因子-κB、缺氧诱导因子-1/血管内皮生长因子、p53等与DR发生发展密切相关的靶基因,产生不同的细胞生物学效应,从而广泛调节视网膜各类细胞在炎症发生、新生血管形成、增生和凋亡等方面的病理过程.异常表达的微小RNA及其功能靶标的发现不仅丰富了对DR发病机制的阐述,也为DR的早期预防和探索基因靶向治疗提供新的突破点.     

microRNAs在糖尿病视网膜病变中作用的研究进展

microRNAs(miRNAs)是一种具有调节基因表达功能的非编码小RNA分子,可以在包括血清或血浆在内的许多生物液中由细胞和组织释放.大量研究已经证实不同的miRNAs在糖尿病视网膜病变(DR)中的表达可特异性增高或减少,最近越来越多的证据表明血清和血浆中某些miRNAs在DR中存在特异性表达并参与DR的发生发展,...     

RNA干扰抑制视网膜母细胞瘤血管内皮生长因子基因的表达

目的利用RNA干扰技术在视网膜母细胞瘤(retinoblastoma,RB)细胞内诱导RNA干扰(RNAi),抑制血管内皮生长因子(vascular endothelial growth factor,VEGF)基因表达,在体外细胞水平探讨RNAi对视网膜母细胞瘤治疗的可行性。方法构建靶向VEGF基因的siRNA(VEGF-siRNA),转导入RB细胞,在瘤细胞内诱导RNAi,采用RT-PCR、细胞增殖抑制实验、Northern杂交等技术检测siRNA处理前后RB细胞增殖及VEGF基因表达变化。结果成功构建了两种抗VEGF基因的shRNA表达载体,RT-PCR发现VEGF-siRNA在RB细胞系中,能明显抑制VEGF基因的表达,抑制率为72%;对RB细胞生长抑制率达47%;VEGF基因的mRNA表达降低了78%。结论VEGF-siRNA在体外能明显抑制了视网膜母细胞瘤细胞增殖和VEGF基因的表达。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.