泪腺腺样囊性癌相关的小RNA及其调控作用

泪腺腺样囊性癌(lacrimal gland adenoid cystic carcinoma, LGACC)是一种常见的、发生于泪腺的恶性上皮性肿瘤, 其复发率和转移率均较高。多种小RNA(miRNA)在LGACC的发生、发展中起重要作用。miR-24-3p过表达可降低LGACC中PRKCH的表达以促进p53/p21表达, 从而抑制肿瘤的侵袭。miR-93-5p通过调控Wnt信号通路, 靶向下调乳腺癌转移抑制因子1L, 而促进LGACC细胞上皮细胞-间充质转化、迁移、侵袭和增生。LGACC中的miR-181a-5p表达上调, 也是LGACC细胞增生和迁移的原因之一。(国际眼科纵览, 2022, 46:157-161)     

外周血液中miRNA表达与老年性黄斑变性相关性研究

目的　检测微小核糖核酸（microribonucleicacids，miRNA）在老年性黄斑变性（age-related macular degeneration，AMD）患者中的表达，并探讨miRNA的表达量与AMD病程之间的关系。方法　选取2014年1月至2016年11月于同济大学附属第十人民医院眼科门诊就诊的AMD患者6例为试验组，并选取同期6名正常人为对照组，通过基因芯片技术检测两组血液中miRNA的表达量。扩大样本的病例对照研究中共纳入126例AMD患者和140名正常人，检测其血液样本中miRNA的表达，比较两组人群间miRNA的表达量差异。结果　通过基因芯片技术，在试验组与对照组间共检测出216个miRNA存在表达差异（均为P<0.05），与对照组相比，试验组中111个miRNA表达量上升，105个miRNA表达量下降，差异均有统计学意义（均为P<0.05）。扩大样本的病例对照研究结果表明，在AMD患者中，miR-27a-3p、miR-29b-3p、miR-195-5p的表达量显著上升，同时，湿性AMD患者血液中miR-27a-3p的表达量高于干性AMD患者，差异均有统计学意义（均为P<0.05）。结论　AMD患者外周血中miRNA表达量水平有明显变化，miR-27a-3p、miR-29b-3p、miR-195-5p可能成为AMD血清学诊断和预后的标志物。     

miRNA-19对葡萄膜黑色素瘤细胞增殖、凋亡、迁移和侵袭的影响及其机制研究

目的 探讨miR-19在葡萄膜黑色素瘤(UM)细胞中的表达及其对UM细胞增殖、凋亡、迁移和侵袭的影响及其作用机制.方法 qRT-PCR检测正常视网膜上皮细胞系ARPE-19和UM细胞系 SP6.5、M23中 miR-19的表达.将 M23细胞分为 miR-19 inhibitor 组(转染 miR-19-inhibit...     

miR-30b-5p 抑制Notch信号通路活化对实验性自身免疫性葡萄膜炎的治疗作用

目的　探讨miR-30b-5p对实验性自身免疫性葡萄膜炎(EAU)大鼠Notch信号通路活化的调控机制及治疗作用。方法　通过Target Scan（http://www.targetscan.org/）对Notch1和Dll4基因与 miR-30b 的关系进行生物信息学预测。将雌性Lewis大鼠随机分为对照组、EAU组、miR-30b-5p组和miR-30b-5p空载体（miR-30b-5p-N）组。EAU组、miR-30b-5p组和miR-30b-5p-N组大鼠首先诱导EAU模型,miR-30b-5p组和miR-30b-5p-N组大鼠分别采用携带miR-30b-5p和miR-30b-5p-N的慢病毒于EAU大鼠脾脏进行注射干预处理,EAU组大鼠于同一部位注射相同体积的生理盐水。处理后12 d,实时荧光定量PCR检测4组大鼠脾脏、淋巴结和眼组织中Notch1和Dll4 mRNA的表达;免疫组织化学检测4组大鼠脾脏、淋巴结及眼组织中Notch1和Dll4蛋白的表达,分析miR-30b-5p对葡萄膜炎大鼠Notch信号通路的调控作用。结果　生物信息学预测分析结果表明,Notch 信号通路上 Notch1和Dll4基因均为 miR-30b 调控的靶基因。免疫后12 d,相比于对照组,EAU组、miR-30b-5p组和miR-30b-5p-N组大鼠脾脏、淋巴结和眼组织中Notch1和Dll4 mRNA水平均升高（均为P<0.05）;经miR-30b-5p干预治疗后,miR-30b-5p组脾脏、淋巴结和眼组织中Notch1和Dll4 mRNA表达均显著降低（均为P<0.05）。免疫组织化学检测结果显示,免疫后12 d,EAU组、miR-30b-5p组和miR-30b-5p-N组大鼠脾脏、淋巴结和眼组织中Notch1和Dll4 蛋白表达均上调（均为P<0.05）;miR-30b-5p干预治疗后,脾脏、淋巴结和眼组织中Notch1和Dll4蛋白表达均显著下调（均为P<0.05）。结论　miR-30b-5p可明显下调EAU大鼠各组织中Notch1和Dll4等Notch信号通路相关分子的表达进而抑制Notch信号通路活化,从而达到治疗葡萄膜炎的作用。     

miR-34a-5p通过调节Nrf2-Keap1信号通路介导年龄相关性白内障氧化应激的实验研究

目的　探讨miR-34a-5p通过调节Nrf2-Keap1信号通路介导年龄相关性白内障的氧化应激。方法　检测年龄相关性白内障患者和正常透明晶状体前囊组织及人晶状体上皮细胞氧化应激模型中miR-34a-5p和预测靶基因Nrf2表达及人晶状体上皮细胞内活性氧（reactive oxygen species，ROS）活性。将miR-34a-5p模拟物、模拟物对照、miR-34a-5p抑制剂和抑制剂对照分别转染人晶状体上皮细胞，然后用400 μmol·L^-1 H₂O₂作用8 h后检测miR-34a-5p、Nrf2 mRNA和Nrf2蛋白表达，并检测人晶状体上皮细胞增殖活性。结果　正常晶状体前囊组织中miR-34a-5p的相对表达量为1.03±0.29，Nrf2 mRNA的相对表达量为1.31±0.39；年龄相关性白内障组织中miR-34a-5p的相对表达量为2.69±0.99，Nrf2 mRNA的相对表达量为0.64±0.25。与正常组织相比，年龄相关性白内障晶状体组织中miR-34a-5p表达显著升高，Nrf2表达显著降低。Nrf2蛋白在年龄相关性白内障晶状体组织中表达也显著降低（均为P<0.001）。在人晶状体上皮细胞氧化应激模型中，miR-34a-5p表达显著升高，靶基因Nrf2表达显著降低，内源性ROS水平显著升高（均为P<0.001）。miR-34a-5p模拟物转染人晶状体上皮细胞后，miR-34a-5p表达显著升高，Nrf2表达显著降低，内源性ROS水平显著升高，细胞增殖活性显著降低（均为P<0.001），然而，miR-34a-5p抑制剂转染人晶状体上皮细胞后，miR-34a-5p表达显著降低，Nrf2表达显著升高，内源性ROS水平显著降低，细胞增殖活性显著升高（均为P<0.001）。双荧光素酶报告分析证实，Nrf2是miR-34a-5p的直接靶点。结论　MiR-34a-5p通过调节Nrf2-Keap1信号通路增加晶状体上皮细胞氧化应激，抑制晶状体上皮细胞的增殖，从而参与年龄相关性白内障的发生发展过程。     

MicroRNA-199a-3p对脉络膜黑色素瘤细胞增殖的抑制作用

目的：探讨MicroRNA-199a-3p（miR-199a-3p）对脉络膜黑色素瘤细胞OCM290增殖的影响及机制。 方法：实验研究。首先采用Real-time PCR技术检测miR-199a-3p在正常的脉络膜黑色素细胞UM96和肿瘤细胞OCM290中的表达情况;其次采用阳离子脂质体Lipofectamine介导的转染方法,将miR- 199a-3p转染入体外培养的人脉络膜黑色素瘤细胞OCM290中过表达作为实验组,将随机序列寡核苷酸链转染入OCM290细胞作为阴性对照组;然后在转染的基础上运用细胞增殖实验法（MTS法）、克隆形成实验检测细胞增殖和生长能力。流式细胞术检测细胞周期。Western blot法检测与细胞周期相关的信号蛋白如CDK2、CDK4、E2F1等的表达。组间数据比较采用独立样本t检验。结果：miR-199a-3p在UM96中高表达,而在OCM290中表达明显下调（t=13.2,P<0.001）。OCM290细胞转染 miR-199a-3p后,MTS结果显示实验组细胞数为对照组的（23.8±1.7）%,细胞增殖明显被抑制（t=78.1,P<0.001);细胞克隆数减少;细胞周期滞留在G1期（t=-8.5,P=0.001）;Western blot法检测发现miR-199a-3p能下调OCM290中CDK2、CDK4、E2F1等的表达水平（t=10.3,P=0.001;t=9.9,P=0.001; t=10.4,P<0.001）。结论：miR-199a-3p通过下调调控细胞周期进程的关键蛋白,影响细胞周期的进程,从而抑制脉络膜黑色素瘤细胞的增殖。     

白塞氏病患者血浆中微小RNA异常表达的初步研究

目的：检测白塞氏病(BD)患者和正常人群血浆中微小核糖核酸(microRNA，miRNA)的差异表达谱，探讨miRNA在BD发病中的作用，寻找与BD相关的血浆生物标记物。

方法：收集15例活动期BD患者和15例正常人的抗凝静脉血，离心获得血浆，提取总RNA，经miRNA标记、miRNA阵列杂交、miRNA阵列扫描和分析获得BD患者异常表达的miRNA谱。通过miRTarBase(靶基因数据库)检索差异性表达的miRNA已经过验证的靶基因，并选取与免疫学相关的差异性表达的miRNA进行Real time-PCR验证。

结果：活动期BD患者血浆中hsa-miR-34c-5p、hsa-miR-144-3p、hsa-miR-483-3p较正常人表达上调，hsa-miR-301a-3p、hsa-miR-224-5p、hsa-miR-454-3p、hsa-miR-17-5p、hsa-miR-199a-5p较正常人表达下调。

结论：miRNA的差异性在BD的发生发展过程发挥重要作用，异常表达的miRNA可能通过Notch1和SMAD4信号通路促进BD发病。     

miR-34a-5p对ARPE-19细胞TGF-β/Smad通路相关蛋白表达及细胞增殖、迁移和上皮-间质转化的影响

目的 探讨miR-34a-5p对ARPE-19细胞TGF-β/Smad通路相关蛋白表达及细胞增殖、迁移和上皮-间质转化(EMT)的影响。方法 将ARPE-19细胞分为4组：对照组、转化生长因子(TGF)-β1组、miR-34a-5p过表达组与复合干预组,对照组与TGF-β1组采用Lipofectamine 2000转染试剂转染对照模拟物,miR-34a-5p过表达组与复合干预组转染miR-34a-5p模拟物,培养24 h后采用无血清培养基饥饿培养12 h, TGF-β1组与miR-34a-5p过表达组均添加10 mg·L^-1的TGF-β1,复合干预组添加10 mg·L^-1的TGF-β1与10μmol·L^-1的TGF-β通路激活剂SRI-011381,各组细胞继续培养24 h,测定细胞增殖、迁移与EMT。采用Western blot检测细胞TGF-β/Smad通路相关蛋白的表达水平,Ki67荧光染色检测细胞增殖情况,免疫荧光染色测定细胞EMT相关蛋白表达情况,划痕实验和Transwell实验测定细胞的迁移和侵袭能力。结果 ...     

叔丁基对苯二酚对糖尿病大鼠视网膜的保护作用及其机制研究

目的　探讨叔丁基对苯二酚（tert-Butylhydroquinone,tBHQ）对糖尿病大鼠视网膜的保护作用及其机制,为DR防治提供新靶点。方法　18只雄性SD大鼠随机分成3组:正常组、糖尿病组（高脂高糖饮食）和tBHQ干预组（高脂高糖饮食中加入质量分数1%tBHQ）,后两组饮食干预4周后建立糖尿病大鼠模型,饮食干预3个月后处死各组大鼠。采集大鼠空腹血用于测定生化和胰岛素相关指标,HE染色观察大鼠视网膜各层组织变化,使用miRNA表达谱芯片测量大鼠视网膜差异性miRNA,实时定量PCR验证特定miRNA在3组大鼠视网膜的表达水平,分析差异性miRNA的相关通路。结果　tBHQ干预组［（15.073±7.079）mmol·L^-1］较正常组［（7.635±1.421）mmol·L^-1］空腹血糖升高（P<0.05）,较糖尿病组［（22.331±1.824）mmol·L^-1］降低（P<0.05）。tBHQ干预组［（47.961±15.256）μU·L^-1］血清胰岛素较正常组［（78.090±20.974）μU·L^-1］减少,而较糖尿病组［（17.533±3.959）μU·L^-1］增多（均为P<0.01）。HE染色结果示,糖尿病组大鼠视网膜出现严重水肿,各层结构不清,tBHQ干预组视网膜改变相对轻微。与糖尿病组大鼠相比,tBHQ干预组视网膜中miR-325-3p（>2.0倍）和miR-551b-3p（>1.5倍）上调,miR-652-3p（>2.0倍）下调。实时定量PCR验证miR-325-3p和miR-551b-3p为差异性miRNA,靶基因预测分析示miR-325-3p可介导21条信号通路。结论　tBHQ可能通过miR-325-3p介导的信号通路对2型糖尿病大鼠视网膜起保护作用。     

转化生长因子-β1在葡萄膜黑色素瘤中的表达及意义

目的:探讨转化生长因子-β(1TGF-β1)在葡萄膜黑色素瘤中的表达及意义。方法:以原位杂交法检测78例葡萄膜黑色素瘤中TGF-β1mRNA的表达,并按WHO1980年的标准进行分型:梭型细胞型,类上皮细胞型和混合细胞型。进行临床随访。结果:78例中,梭型细胞型21例,类上皮细胞型34例,混合细胞型23例。TGF-β1mRNA在3种类型的葡萄膜黑色素瘤中均有不同程度的表达,表达强度随梭型细胞型,混合细胞型和类上皮细胞型依次递增。回访37例患者,其中梭型细胞型18例,平均生存时间为(78.3±14.2)mo,混合细胞型10例,平均生存时间(69.1±17.4)mo,类上皮细胞型9例,平均生存时间(36.8±12.2)mo。患者生存时间与TGF-β1表达强度呈负相关。结论:TGF-β1可能在葡萄膜黑色素瘤的转移,浸润中发挥重要作用。     

Analysis of MicroRNA Expression in Tears of Patients with Herpes Epithelial Keratitis: A Preliminary Study

PurposeHerpes epithelial keratitis (HEK) is the most common form of herpes simplex virus (HSV) eye involvement, and understanding the molecular mechanisms underlying HEK is important. We investigated the expression of microRNAs (miRNAs) in the tears of patients with HEK.MethodsTear samples from eight patients with HEK and seven age-matched controls were evaluated. Clinical ophthalmologic evaluation was performed, and an anterior segment photograph was obtained after fluorescence staining. Dendritic or geographic ulcer areas were measured using ImageJ software. The expression of 43 different miRNAs in tears was measured using real-time polymerase chain reaction and compared between patients with HEK and controls. Differences in miRNA expression between the dendritic and geographic ulcer groups and correlations involving miRNA expression and ulcer area were evaluated.ResultsOf the 43 miRNAs, 23 were upregulated in patients with HEK compared to normal controls. MiR-15b-5p, miR-16-5p, miR-20b-5p, miR-21-5p, miR-23b-3p, miR-25-3p, miR-29a-3p, miR-30a-3p, miR-30d-5p, miR-92a-3p, miR-124-3p, miR-127-3p, miR-132-3p, miR-142-3p, miR-145-5p, miR-146a-5p, miR-146b-5p, miR-155-5p, miR-182-5p, miR-183-5p, miR-221-3p, miR-223-3p, and miR-338-5p were significantly upregulated in patients with HEK. MiR-29a-3p exhibited significant differences between the dendritic and geographic ulcer groups. All 23 miRNAs with significant differences between patients with HEK and the control group were not significantly correlated with ulcer area.ConclusionsTwenty-three miRNAs were significantly upregulated in the tears of patients with HEK, and the expression of miRNAs may play important roles in herpes infection in relation to host immunity.     

Expression of microRNAs in fibroblast of pterygium

AIM: To screen microRNAs (miRNAs) and set up target miRNAs in pterygium. METHODS: Primary fibroblasts were isolated from pterygium and Tenon''s capsule and cultured. Immunocytochemical analysis and Western blotting were performed to confirm the culture of fibroblasts. In all, 1733 miRNAs were screened in the first step by using GeneChip® miRNA3.0 Array. Specific miRNAs involved in the pathogenesis of pterygium were subsequently determined using the following criteria: 1) high reproducibility in a repetitive test; 2) base log value of >7.0 for both control and pterygial fibroblasts; and 3) log ratio of >1.0 between pterygial fibroblasts and control fibroblasts. RESULTS: Primary screening showed that 887/1733 miRNAs were up-regulated and 846/1733 miRNAs were down-regulated in pterygial fibroblasts compared with those in control fibroblasts. Of the 1733 miRNAs screened, 4 miRNAs, namely, miRNA-143a-3p, miRNA-181a-2-3p, miRNA-377-5p and miRNA-411a-5p, met the above-mentioned criteria. Primary screening showed that these 4 miRNAs were up-regulated in pterygial fibroblasts compared with control fibroblasts and that miRNA-143a-3p had the highest mean ratio compared with the miRNAs in control fibroblasts. CONCLUSION: miRNA-143a-3p, miRNA-181a-2-3p, miRNA-377-5p and miRNA-411a-5p are up-regulated in pterygial fibroblasts compared with control fibroblasts, suggesting their involvement in the pathogenesis of pterygium.     

Long Noncoding RNA 3632454L22Rik Contributes to Corneal Epithelial Wound Healing by Sponging miR-181a-5p in Diabetic Mice

PurposeThis work explores the abnormal expression of long noncoding RNAs (lncRNAs), microRNAs (miRNAs) and messenger RNAs (mRNAs) in diabetic corneal epithelial cells (CECs) and constructs an associated competitive endogenous RNA (ceRNA) network. Moreover, we revealed that Rik may exert advantageous effects on diabetic corneal epithelial wound closure by sponging miR-181a-5p.MethodsWe obtained the profiles of differentially expressed lncRNAs (DELs) of CECs of type 1 diabetic versus control corneas by microarray and summarized the differentially expressed miRNAs (DEmiRs) and differentially expressed genes (DEGs) data by published literature. Subsequently, the ceRNA network was constructed using bioinformatics analyses. The levels of lncRNA ENSMUST00000153610/3632454L22Rik (Rik) and miR-181a-5p were verified. The localization of Rik was identified with fluorescence in situ hybridization (FISH), and dual-luciferase assays proved the targeted relationship between Rik and miR-181a-5p. Furthermore, we validated the functional impact of Rik in vitro.ResultsOverall, 111 upregulated and 117 downregulated DELs were detected in diabetic versus control CECs. The level of Rik located in both the cytoplasm and the nucleus was clearly downregulated, whereas miR-181a-5p was upregulated in vitro and in vivo in the diabetic group versus the control group. Rik can act as a ceRNA to bind to miR-181a-5p, thus promoting diabetic corneal epithelial wound healing in vitro.ConclusionsThis work investigated the expression profile of DELs and constructed ceRNA networks of diabetic CECs for the first time. Furthermore, we revealed that Rik may positively impact diabetic corneal epithelial wound healing by sponging miR-181a-5p, providing a novel potential therapeutic target of diabetic keratopathy (DK).     

Identification of differentially expressed metastatic genes and their signatures to predict the overall survival of uveal melanoma patients by bioinformatics analysis

AIM: To identify metastatic genes and miRNAs and to investigate the metastatic mechanism of uveal melanoma (UVM). METHODS: GSE27831, GSE39717, and GSE73652 gene expression profiles were downloaded from the Gene Expression Omnibus (GEO) database, and the limma R package was used to identify differentially expressed genes (DEGs). Gene Ontology (GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed using the DAVID online tool. A comprehensive list of interacting DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) database and Cytoscape software. The Cytoscape MCODE plug-in was used to identify clustered sub-networks and modules of hub genes from the protein-protein interaction network. GEPIA online software was used for survival analysis of UVM patients (n=80) from the The Cancer Genome Atlas (TCGA) cohort. OncomiR online software was used to find that the miRNAs were associated with UVM prognosis from the TCGA cohort. TargetScan Human 7.2 software was then used to identify the miRNAs targeting the genes. RESULTS: There were 1600 up-regulated genes and 1399 down-regulated genes. The up-regulated genes were mainly involved in protein translation in the cytosol, whereas the down-regulated genes were correlated with extracellular matrix organization and cell adhesion in the extracellular space. Among the 2999 DEGs, five genes, Znf391, Mrps11, Htra3, Sulf2, and Smarcd3 were potential predictors of UVM prognosis. Otherwise, three miRNAs, hsa-miR-509-3-5p, hsa-miR-513a-5p, and hsa-miR-1269a were associated with UVM prognosis. CONCLUSION: After analyzing the metastasis-related enriched terms and signaling pathways, the up-regulated DEGs are mainly involved in protein synthesis and cell proliferation by ribosome and mitogen-activated protein kinase (MAPK) pathways. However, the down-regulated DEGs are mainly involved in processes that reduced cell-cell adhesion and promoted cell migration in the extracellular matrix through PI3K-Akt signaling pathway, focal adhesion, and extracellular matrix-receptor interactions. Bioinformatics and interaction analysis may provide new insights on the events leading up to the development and progression of UVM.     

Simple transscleral fixation of IOL technique without tying up haptics

AIM: To identify metastatic genes and miRNAs and to investigate the metastatic mechanism of uveal melanoma (UVM). METHODS: GSE27831, GSE39717 and GSE73652 gene expression profiles were downloaded from the Gene Expression Omnibus (GEO) database, and the limma R package was used to identify differentially expressed genes (DEGs). Gene Ontology (GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed using the DAVID online tool. A comprehensive list of interacting DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) database and Cytoscape software. The Cytoscape MCODE plug-in was used to identify clustered sub-networks and modules of hub genes from the protein-protein interaction network. GEPIA online software was used for survival analysis of UVM patients (n=80) from the The Cancer Genome Atlas (TCGA) cohort. OncomiR online software was used to find that the miRNAs were associated with UVM prognosis from the TCGA cohort. TargetScan Human 7.2 software was then used to identify the miRNAs targeting the genes. RESULTS: There were 1600 up-regulated genes and 1399 down-regulated genes. The up-regulated genes were mainly involved in protein translation in the cytosol, whereas the down-regulated genes were correlated with extracellular matrix organization and cell adhesion in the extracellular space. Among the 2999 DEGs, five genes, Znf391, Mrps11, Htra3, Sulf2, and Smarcd3 were potential predictors of UVM prognosis. Otherwise, three miRNAs, hsa-miR-509-3-5p, hsa-miR-513a-5p, and hsa-miR-1269a were associated with UVM prognosis. CONCLUSION: After analyzing the metastasis-related enriched terms and signaling pathways, the up-regulated DEGs are mainly involved in protein synthesis and cell proliferation by ribosom and mitogen-activated protein kinase (MAPK) pathways. However, the down-regulated DEGs are mainly involved in processes that reduced cell-cell adhesion and promoted cell migration in the extracellular matrix through PI3K-Akt signaling pathway, focal adhesion, and extracellular matrix-receptor interactions. Bioinformatics and interaction analysis may provide new insights on the events leading up to the development and progression of UVM.     

Altered microRNA expression profiles in retinas with diabetic retinopathy

Rats with streptozotocin (STZ)-induced diabetes were studied in order to identify abnormal microRNA (miRNA) expression profiles in diabetic retinopathy (DR) and to ascertain miRNAs associated with DR. Histopathologically, we observed characteristic features of DR in rats at 10 weeks after STZ injection. Investigation of miRNA expression profiles in the retinas of control and diabetic rats using miRNA microarrays revealed that many miRNAs were abnormally expressed in DR. On the basis of their fold changes and probability values, a total of 37 miRNAs were selected for further validation by real-time PCR analysis. The results showed that 11 miRNAs were significantly upregulated and 6 miRNAs were notably downregulated in DR. Furthermore, these changes in retinal miRNA expression levels paralleled the course of DR. Levels of miR-182, miR-96, miR-183, miR-211, miR-204, and miR-124 were significantly increased during the progress of DR, whereas miR-10b, miR-10a, miR-219-2-3p, miR-144, miR-338, and miR-199a-3p were significantly decreased. Our data indicate that the aberrant miRNA expression profiles in DR are associated with the development of DR. Modulation of retinal miRNA expression levels may provide a potential therapeutic strategy for DRs.