Long Noncoding RNA <i>OIP5-AS1</i> Promotes Cell Apoptosis and Cataract Formation by Blocking <i>POLG</i> Expression Under Oxidative Stress

Jing, Ruihua; Ma, Bo; Qi, Tiantian; Hu, Conghui; Liao, Chongbing; Wen, Chuangyu; Shao, Yongping; Pei, Cheng

doi:10.1167/iovs.61.12.3

Cited by 21 publications

(14 citation statements)

References 59 publications

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Section: A Single Lncrna: a Myriad Diseasesmentioning

confidence: 99%

“…OIP5‐AS1 has been implicated in the development of cataracts, where under oxidative stress, it is activated by TFAP2A and upregulated in B3 cells and lens epithelial cells 73 . Knockdown of OIP5‐AS1 resulted in a reduction of B3 cell apoptosis due to H 2 O 2 ‐induced oxidative stress, as well as an absence of lens opacity under oxidative stress, all of which contribute to the development of cataracts 73 . The hypothesis is that OIP5‐AS1 contributes to regulation of the HuR‐mediated mitochondrial apoptosis pathway in B3 cells by mediating the destruction of POLG mRNA in the presence of oxidative stress, which could support the eventual development of cataracts 73 …”

Section: A Single Lncrna: a Myriad Diseasesmentioning

confidence: 99%

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Long non‐coding RNA OIP5‐AS1 (Cyrano): A context‐specific regulator of normal and disease processes

Wooten

Smith

2022

Clinical & Translational Med

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Long non‐coding (lnc) RNAs have been implicated in a plethora of normal biological functions, and have also emerged as key molecules in various disease processes. OIP5‐AS1, also commonly known by the alias Cyrano, is a lncRNA that displays broad expression across multiple tissues, with significant enrichment in particular contexts including within the nervous system and skeletal muscle. Thus far, this multifaceted lncRNA has been found to have regulatory functions in normal cellular processes including cell proliferation and survival, as well as in the development and progression of a myriad disease states. These widespread effects on normal and disease states have been found to be mediated through context‐specific intermolecular interactions with dozens of miRNAs and proteins identified to date. This review explores recent studies to highlight OIP5‐AS1's contextual yet pleiotropic roles in normal homeostatic functions as well as disease oetiology and progression, which may influence its utility in the generation of future theranostics.

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Section: A Single Lncrna: a Myriad Diseasesmentioning

confidence: 99%

Section: A Single Lncrna: a Myriad Diseasesmentioning

confidence: 99%

Long non‐coding RNA OIP5‐AS1 (Cyrano): A context‐specific regulator of normal and disease processes

Wooten

Smith

2022

Clinical & Translational Med

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“…Cyrano a lncRNA namely OIP5-AS1 works in vivo as an up-regulating system, with the capacity of renewal embryonic stem cells, modulating miR7 MicroRNAs (miRNAs, miR), capable of regulating post-transcriptional gene expressions; disproportion in the miRNA network has been associated with the development of many pathological conditions and diseases, including not only cataracts but cancer [86][87][88][89].…”

Section: Oxidative Stress As a Key Element In Cataract Formationmentioning

confidence: 99%

Reactive Oxygen Species and Eye Aging in Cataracts through Biomolecular Mechanisms

Pacheco

2022

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The cataractogenesis process and the novel mechanisms involved in its progression make us question that the only solution today presented for its resolution is through a surgical procedure. The unveiling of such interesting and intricate machinery in the lens opacification occupies not only the ophthalmologists field, but also biology, molecular, and biochemistry areas. The animal models, experimental and theoretically, have done their best try to present what appears to be an irreparable and unstoppable process nowadays. The crystalline lens opacification is chronic and progressively damaged due to the loss of balance between the production and elimination of free reactive oxygen species (ROS), the attempts to stop or slow down this overproduction or lack of elimination lie in study material from disciplines as complex as cancer pathways. The execution of this review article was possible through metasearch engines like Wiley Online Library, EBSCO, Cochrane, Clinical key and MEDLINE PubMed (National Library of Medicine, National Institutes of Health), to retrieve studies from January 2021 to January 2022, following PRISMA guidelines, with a special affinity to systematic reviews and meta-analysis. MeSH Terms associated with "Cataract AND Reactive Oxygen Species". This work constitutes an integral cataractogenesis view in the development of future therapeutic scopes. The world population especially in Europe is aging at a rapid rate, in this sense is necessary to consider a root potential solution and not palliative strategies in ophthalmology for the next generations. The compendium of procedures presented already supposed to open a new panorama to a clearer world, a world without senile cataracts. Time is vision.

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“…Studies have found that although long non-coding RNAs (LncRNAs) cannot directly encode proteins, they can regulate the expression of apoptosis-related genes before, during, and after gene transcription, thereby interfering with apoptosis [11][12][13][14]. To determine which LncRNAs are related to the hypoxic apoptosis of BMSCs, we used LncRNA chip combined with bioinformatics analysis.…”

Section: Introductionmentioning

confidence: 99%

Hypoxic condition induced H3K27me3 modification of the LncRNA Tmem235 promoter thus supporting apoptosis of BMSCs

et al. 2022

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Bone marrow mesenchymal stem cells (BMSCs) have strong regenerative potential and show good application prospects for treating clinical diseases. However, in the process of BMSC transplantation for treating ischemic and hypoxic diseases, BMSCs have high rates of apoptosis in the hypoxic microenvironment of transplantation, which significantly affects the transplantation efficacy. Our previous studies have confirmed the key role of long non-coding RNA Tmem235 (LncRNA Tmem235) in the process of hypoxia-induced BMSC apoptosis and its downstream regulatory mechanism, but the upstream mechanism by which hypoxia regulates LncRNA Tmem235 expression to induce BMSC apoptosis is still unclear. Under hypoxic conditions, we found that the level of LncRNA Tmem235 promoter histone H3 lysine 27 trimethylation modification (H3K27me3) was significantly increased by CHIP-qPCR. Moreover, H3K27me3 cooperated with LncRNA Tmem235 promoter DNA methylation to inhibit the expression of LncRNA Tmem235 and promote apoptosis of BMSCs. To study the mechanism of hypoxia-induced modification of LncRNA Tmem235 promoter H3K27me3 in the hypoxia model of BMSCs, we detected the expression of H3K27 methylase and histone demethylase and found that only histone methylase enhancer of zeste homolog 2 (EZH2) expression was significantly upregulated. Knockdown of EZH2 significantly decreased the level of H3K27me3 modification in the LncRNA Tmem235 promoter. The EZH2 promoter region contains a hypoxia-responsive element (HRE) that interacts with hypoxia-inducible factor-1alpha (HIF-1α), which is overexpressed under hypoxic conditions, thereby promoting its overexpression. In summary, hypoxia promotes the modification of the LncRNA Tmem235 promoter H3K27me3 through the HIF-1α/EZH2 signaling axis, inhibits the expression of LncRNA Tmem235, and leads to hypoxic apoptosis of BMSCs. Our findings improve the regulatory mechanism of LncRNA Tmem235 during hypoxic apoptosis of BMSCs and provide a more complete theoretical pathway for targeting LncRNA to inhibit hypoxic apoptosis of BMSCs.

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Long Noncoding RNA OIP5-AS1 Promotes Cell Apoptosis and Cataract Formation by Blocking POLG Expression Under Oxidative Stress

Cited by 21 publications

References 59 publications

Long non‐coding RNA OIP5‐AS1 (Cyrano): A context‐specific regulator of normal and disease processes

Long non‐coding RNA OIP5‐AS1 (Cyrano): A context‐specific regulator of normal and disease processes

Reactive Oxygen Species and Eye Aging in Cataracts through Biomolecular Mechanisms

Hypoxic condition induced H3K27me3 modification of the LncRNA Tmem235 promoter thus supporting apoptosis of BMSCs

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