The Long-Noncoding RNA TUG1 Regulates Oxygen-Induced Retinal Neovascularization in Mice via MiR-299

Wang, Yue; Wang, Xue; Wang, Yuexia; Ma, Yuan; Di, Yu

doi:10.1167/iovs.63.1.37

Cited by 13 publications

(10 citation statements)

References 46 publications

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“…These results indicate that miR-145-5p overexpression has a protective effect on RNV/OIR. Moreover, we have previously demonstrated that knocking down TUG1 can reduce retinal apoptosis, inflammation, and damage in OIR mice ( 33 ). In conclusion, TUG1 acts as a molecular sponge of miR-145-5p to regulate CCN1 expression and TUG1/miR-145-5p/CCN1 together are involved in the occurrence and development of RNV in OIR mice.…”

Section: Discussionmentioning

confidence: 99%

LncRNA TUG1 Promotes Apoptosis, Invasion, and Angiogenesis of Retinal Endothelial Cells in Retinopathy of Prematurity via MiR-145-5p

Wang

et al. 2022

Front. Med.

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PurposeRetinopathy of prematurity (ROP) is a common retinal vascular disease in premature neonates. In recent years, there is increasing evidence that the long non-coding RNA taurine upregulated gene 1 (TUG1) plays a regulatory role in vascular diseases, suggesting a potential role for TUG1 in vascular endothelial cells. We hypothesized that TUG1 may be associated with ROP. Our aim, therefore, was to explore the biological functions of TUG1 in aberrant retinal development.MethodsWe used the mouse oxygen-induced retinopathy (OIR) model to simulate the pathological changes of retinal in ROP. Quantitative real-time polymerase chain reaction was used to detect the expression of TUG1, miR-145-5p and cellular communication network factor 1 (CCN1). Human retinal endothelial cells (HRECs) were treated with CoCl2 to mimic hypoxia conditions. Cellular functional changes were observed after transfection with RNA interference (RNAi)-TUG1 and miR-145-5p mimics. The apoptosis of HRECs was detected by flow cytometry, the migration ability was detected by wound healing and transwell migration assays, and the ability of angiogenesis was detected by tube formation assay. The potential binding sites between TUG1, miR-145-5p, and CCN1 were verified by dual-luciferase reporter assays. The degree of retinopathy was evaluated by staining retinal sections with hematoxylin and eosin, and the expression of CCN1, HIF-1α, VEGF, caspase-3, Bcl-2, IL-1β, and TNF-α protein was analyzed by Western blotting and immunohistochemistry.ResultsIn the retina tissue of OIR mice, TUG1, miR-145-5p, and CCN1 were differentially expressed. Knocking down TUG1 attenuated apoptosis, migration, and angiogenesis induced by hypoxia on HRECs, as did miR-145-5p overexpression. Results from reporter assays indicate direct interactions between TUG1, miR-145-5p, and CCN1. Intravitreal injection of miR-145-5p mimics reduced the degree of retinopathy.ConclusionTUG1 acts as a molecular sponge of miR-145-5p to regulate CCN1 expression and thus regulate the development of retinal neovascularization. This regulatory mechanism may provide a new theoretical basis for the prevention and treatment of ROP.

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Section: Discussionmentioning

confidence: 99%

LncRNA TUG1 Promotes Apoptosis, Invasion, and Angiogenesis of Retinal Endothelial Cells in Retinopathy of Prematurity via MiR-145-5p

Wang

et al. 2022

Front. Med.

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“…TUG1, another long non-coding RNA, is also involved in oxygen-induced RNV. Knocking down TUG1 suppresses retinal angiogenesis by sponging miR-299-3p, subsequently reducing VEGF-A levels and RNV [ 126 ].…”

Section: Potential Therapeutics and Therapeutic Strategies Of Ropmentioning

confidence: 99%

New Aspects on the Treatment of Retinopathy of Prematurity: Currently Available Therapies and Emerging Novel Therapeutics

Ryu

2022

IJMS

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Retinopathy of prematurity (ROP) is a rare proliferative ocular disorder in preterm infants. Because of the advancements in neonatal care, the incidence of ROP has increased gradually. Now, ROP is one of the leading causes of blindness in children. Preterm infants with immature retinal development are exposed to supplemental oxygen inside an incubator until their cardiopulmonary system is adequately developed. Once they are returned to room air, the relatively low oxygen level stimulates various angiogenesis factors initiating retinal neovascularization. If patients with ROP are not offered adequate and timely treatment, they can experience vision loss that may ultimately lead to permanent blindness. Although laser therapy and anti-vascular endothelial growth factor agents are widely used to treat ROP, they have limitations. Thus, it is important to identify novel therapeutics with minimal adverse effects for the treatment of ROP. To date, various pharmacologic and non-pharmacologic therapies have been assessed as treatments for ROP. In this review, the major molecular factors involved in the pathogenesis of ROP, currently offered therapies, therapies under investigation, and emerging novel therapeutics of ROP are discussed.

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“…Lastly, Wang et al explored the function of lncRNA TUG1 in retinal angiogenesis ( Wang et al, 2022 ). Previously, lncRNA TUG1 was studied in various cancer; however, its role in retinal angiogenesis was not investigated.…”

Section: Noncoding Rna Studies In Retinopathy Of Prematuritymentioning

confidence: 99%

Noncoding RNAs as a novel approach to target retinopathy of prematurity

Kim

Kim²,

Ryu³

2022

Front. Pharmacol.

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Retinopathy of prematurity (ROP), a vascular disease characterized by abnormal vessel development in the retina, has become a primary cause of blindness in children around the world. ROP can be developed during two different phases: vessel loss and vessel proliferation. Once preterm infants with immature retinal vessel growth are exposed to high level of oxygen inside the incubator, vessel loss can occur. When infants are exposed to room air, they may experience the proliferation of vessels in the retina. Although multiple factors are reported to be involved in the pathogenesis of ROP, including vaso-endothelial growth factors (VEGFs) and hypoxia-inducible factors, the pathogenesis of ROP is not completely understood. Although laser therapy and pharmacologic agents, such as anti-VEGF agents, have been commonly used to treat ROP, the incidence of ROP is rapidly rising. Given that current therapies can be invasive and long-term effects are not fully known, the search for novel therapeutic targets with less destructive properties needs to be considered. Within the last decade, the field of noncoding RNA therapy has shown potential as next-generation therapy to treat diverse diseases. In this review, we introduce various noncoding RNAs regulating ROP and discuss their role as potential therapeutic targets in ROP.

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The Long-Noncoding RNA TUG1 Regulates Oxygen-Induced Retinal Neovascularization in Mice via MiR-299

Cited by 13 publications

References 46 publications

LncRNA TUG1 Promotes Apoptosis, Invasion, and Angiogenesis of Retinal Endothelial Cells in Retinopathy of Prematurity via MiR-145-5p

LncRNA TUG1 Promotes Apoptosis, Invasion, and Angiogenesis of Retinal Endothelial Cells in Retinopathy of Prematurity via MiR-145-5p

New Aspects on the Treatment of Retinopathy of Prematurity: Currently Available Therapies and Emerging Novel Therapeutics

Noncoding RNAs as a novel approach to target retinopathy of prematurity

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