Long non-coding RNA MEG3 silencing protects against light-induced retinal degeneration

Zhu, Yunxi; Yao, Jin; Liu, Chang; Hu, Haitao; Li, Xiu‐Miao; Ge, Huan; Zhou, Yunfan; Shan, K. Y.; Jiang, Qin; Yan, Biao

doi:10.1016/j.bbrc.2018.01.177

Cited by 29 publications

(18 citation statements)

References 30 publications

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“…Many miRNAs, lncRNAs and circRNAs have already been successfully been shown to serve as biomarkers or therapeutic targets for numerous different diseases 30 – 32 . Among them, several eye–related pathologies have already been correlated to alterations of ncRNAs, such as retinitis pigmentosa (RP) and other retinal degenerations 33 – 35 , supported by several transcriptomic experiments on retinal pigment epithelium (RPE) cells 36 – 39 . In our work, we compared lncRNA and piRNA expression changes between a group of RPE cells exposed to the oxidant agent oxidized low-density lipoprotein (oxLDL) and another untreated group, considering four time points (1 h, 2 h, 4 h, 6 h) over basal one (time zero).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Non-coding RNAome of RPE cells under oxidative stress suggests unknown regulative aspects of Retinitis pigmentosa etiopathogenesis

Donato

Scimone

Rinaldi

et al. 2018

Sci Rep

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The discovery of thousands of non-coding RNAs has revolutionized molecular biology, being implicated in several biological processes and diseases. To clarify oxidative stress role on Retinitis pigmentosa, a very heterogeneous and inherited ocular disorder group characterized by progressive retinal degeneration, we realized a comparative transcriptome analysis of human retinal pigment epithelium cells, comparing two groups, one treated with oxLDL and one untreated, in four time points (1 h, 2 h, 4 h, 6 h). Data analysis foresaw a complex pipeline, starting from CLC Genomics Workbench, STAR and TopHat2/TopHat-Fusion alignment comparisons, followed by transcriptomes assembly and expression quantification. We then filtered out non-coding RNAs and continued the computational analysis roadmap with specific tools and databases for long non-coding RNAs (FEELnc), circular RNAs (CIRCexplorer, UROBORUS, CIRI, KNIFE, CircInteractome) and piwi-interacting RNAs (piRNABank, piRNA Cluster, piRBase, PILFER). Finally, all detected non-coding RNAs underwent pathway analysis by Cytoscape software. Eight-hundred and fifty-four non-coding RNAs, between long non-coding RNAs and PIWI-interacting, were differentially expressed throughout all considered time points, in treated and untreated samples. These non-coding RNAs target host genes involved in several biochemical pathways are related to compromised response to oxidative stress, visual functions, synaptic impairment of retinal neurotransmission, impairment of the interphotoreceptor matrix and blood – retina barrier, all leading to retinal cell death. These data suggest that non-coding RNAs could play a relevant role in Retinitis pigmentosa etiopathogenesis.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Non-coding RNAome of RPE cells under oxidative stress suggests unknown regulative aspects of Retinitis pigmentosa etiopathogenesis

Donato

Scimone

Rinaldi

et al. 2018

Sci Rep

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“…Long non-coding RNAs (lncRNAs) are a class of RNAs longer than 200 nucleotides that regulate cell apoptosis, oxidative stress, immune responses and inflammation thus to involve in visual maintenance and impairment [14,15]. Researchers observed that in the developing and adult retinal tissues, lncRNA TUG1 was expressed to promote rod photoreceptors production, and in the newborn retina, TUG1 knockdown led to malformed or absent outer segments of photoreceptors, which inhibited the development of retina [16].…”

Section: Introductionmentioning

confidence: 99%

Chlorogenic acid relieved oxidative stress injury in retinal ganglion cells through IncRNA-TUG1/Nrf2

Gong

Zhu

et al. 2019

Cell Cycle

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Objective: To discover the possible underlying mechanism of Chlorogenic acid (CGA) in protecting against oxidative stress injury in glaucoma. Methods: LncRNA TUG1 and Nrf2 expressions were detected by qRT-PCR and Western blot. Retinal ganglion cell (RGC) viability and apoptosis were measured by MTT and flow cytometry, respectively. Reactive oxygen species (ROS) level was determined by reactive oxygen species assay kit. The interaction between lncRNA TUG1 and Nrf2 was confirmed by RNA pull-down and RIP assay. Results: IPL thickness and lncRNA TUG1 expression were significantly decreased in glaucoma mice model, and CGA treatment increased IPL thickness and lncRNA TUG1 expression. In vitro H2O2induced RGCs, RGC viability was significantly decreased, and ROS level and cell apoptosis were significantly increased. CGA up-regulated lncRNA TUG1 and Nrf2 expressions, decreased cell apoptosis and ROS production in RGCs, and increased RGCs viability. We further verified the interaction between lncRNA TUG1 and Nrf2, and proved Nrf2 was positively regulated by lncRNA TUG1. We found CGA promoted Nrf2 expression through lncRNA-TUG1, and further verified CGA protected RGCs from oxidative stress through regulating lncRNA TUG1/Nrf2. In vivo experiments showed TUG1 knockdown abrogated therapeutic effect of CGA on glaucoma. Conclusion: CGA increased RGC viability and decreased ROS level and RGC apoptosis after oxidative stress injury through lncRNA TUG1/Nrf2 pathway, which protected against glaucoma.

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“…As MEG3 was mainly expressed in the cytoplasm, the authors speculated that it might act as a sponge for miRNAs, including miR-7-5p, which was important for RPE changes and AMD progression through the interaction with PAX6, which is important for the RPE differentiation by mediating pigmentation and hyperproliferation in the transdifferentiated RPE [77]. In line with that study is the work of Zhu et al, who showed that MEG3 was upregulated after prolonged and intense light exposure in the retinas of 2-month-old male C57BL/6 mice and the 661W murine photoreceptor cell line [59]. MEG3 silencing with shRNA protected against light-induced retinal damage in mice and apoptosis in the photoreceptor cell line.…”

Section: Long Non-coding Rnas In Amd Modelsmentioning

confidence: 61%

“…Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is expressed in all retinal layers, and its expression is increased in stress conditions in Müller cells and retinal ganglion cells [58]. Another lncRNA counteracting stress condition in the retina is MEG3 (maternally expressed gene 3) [59].…”

Section: Long Non-coding Rnas In Retinal Developmentmentioning

confidence: 99%

Potential of Long Non-Coding RNAs in Age-Related Macular Degeneration

Błasiak

Hyttinen

Szczepańska

et al. 2021

IJMS

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Age-related macular degeneration (AMD) is the leading cause of visual impairment in the aging population with poorly known pathogenesis and lack of effective treatment. Age and family history are the strongest AMD risk factors, and several loci were identified to contribute to AMD. Recently, also the epigenetic profile was associated with AMD, and some long non-coding RNAs (lncRNAs) were shown to involve in AMD pathogenesis. The Vax2os1/2 (ventral anterior homeobox 2 opposite strand isoform 1) lncRNAs may modulate the balance between pro- and anti-angiogenic factors in the eye contributing to wet AMD. The stress-induced dedifferentiation of retinal pigment epithelium cells can be inhibited by the ZNF503-AS1 (zinc finger protein 503 antisense RNA 2) and LINC00167 lncRNAs. Overexpression of the PWRN2 (Prader-Willi region non-protein-coding RNA 2) lncRNA aggravated RPE cells apoptosis and mitochondrial impairment induced by oxidative stress. Several other lncRNAs were reported to exert protective or detrimental effects in AMD. However, many studies are limited to an association between lncRNA and AMD in patients or model systems with bioinformatics. Therefore, further works on lncRNAs in AMD are rational, and they should be enriched with mechanistic and clinical studies to validate conclusions obtained in high-throughput in vitro research.

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Long non-coding RNA MEG3 silencing protects against light-induced retinal degeneration

Cited by 29 publications

References 30 publications

RETRACTED ARTICLE: Non-coding RNAome of RPE cells under oxidative stress suggests unknown regulative aspects of Retinitis pigmentosa etiopathogenesis

RETRACTED ARTICLE: Non-coding RNAome of RPE cells under oxidative stress suggests unknown regulative aspects of Retinitis pigmentosa etiopathogenesis

Chlorogenic acid relieved oxidative stress injury in retinal ganglion cells through IncRNA-TUG1/Nrf2

Potential of Long Non-Coding RNAs in Age-Related Macular Degeneration

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