LncRNA UCA1 Suppresses the Inflammation Via Modulating miR-203-Mediated Regulation of MEF2C/NF-κB Signaling Pathway in Epilepsy

Yu, Qing; Zhao, Mengwen; Yang, Pu

doi:10.1007/s11064-019-02952-9

Cited by 39 publications

(32 citation statements)

References 46 publications

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“…While the molecular mechanisms underlying increased expression of UCA1 are not well understood, the antiinflammatory effect of aspirin could be a determining factor for this. As already mentioned, the relationship between UCA1 and inflammatory pathways has been reported in several studies [26,27], and the protective effects of aspirin on colon and lung cancers through modulation of some lncRNAs have previously been suggested [28,29]. Aspirin is known as a nonsteroidal antiinflammatory drug, and it has also been reported that at the antiplatelet activity dose, it can change cyclooxygenase-2 or COX-2 to the antiinflammatory mediator 15-epi-lipoxin.…”

Section: Discussionmentioning

confidence: 87%

“…It was reported that aspirin could prevent the production of proinflammatory cytokines (IL-6 and TNF-α) via direct inhibition of the IκB/NF-κB pathway [31,32]. LncRNA UCA1 can also suppress inflammation via inhibition of NF-κB and the myocyte-specific enhancer factor 2C (MEF2C)/NF-κB signaling pathway by influencing the production of IL-6, TNF-α and miR-203 [26]. Therefore, we concluded that in response to aspirin, increased levels of UCA1 can act as a compensatory mechanism to decrease the level of TNF-α, as summarized in Fig.…”

Section: Discussionmentioning

confidence: 99%

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Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Nowrouzi-Sohrabi

Seghatoleslam

Izadpanah

et al. 2020

ARCH BIOL SCI BELGRA

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The aim of this study was to investigate the expression of long non-coding RNA urothelial carcinoma-associated 1 (UCA1) and its role in TNF-? production as one of the main inflammatory cytokines, in peripheral blood mononuclear cells (PBMCs) of patients with coronary artery disease (CAD) and healthy non-CAD (NCAD) individuals as the control group. Fifteen CAD and 15 NCAD individuals were enrolled in the study. UCA1 expression in PBMCs and the plasma concentrations of interleukin (IL)-6, IL-22 and tumor necrosis factor (TNF)-? were assessed by real-time PCR and flow cytometry, respectively. UCA1 expression was not significantly different between the CAD and NCAD groups, however, its level was higher in PBMCs of regular aspirin users of both study groups. Furthermore, aspirin users showed a significantly lower plasma level of TNF-? in comparison to nonaspirin users. In addition, UCA1 expression was negatively correlated with the level of TNF-? in the total sample of the examined population. It seems that the increased levels of UCA1 may be an underlying mechanism for down regulation of TNF-? in aspirin users.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Nowrouzi-Sohrabi

Seghatoleslam

Izadpanah

et al. 2020

ARCH BIOL SCI BELGRA

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“…Epilepsy is a neurological disorder that causes imbalance of inhibitory and excitatory neurons in the CNS (24). The activation of astrocytes and inflammation are associated with epileptogenesis and its frequency in patients with epilepsy, which may further result in damage or necrosis of brain neurons (12,25,26). Astrocytes have specific glutamate transporters include GLT1 and GLAST are responsible for glutamate uptake and maintain normal levels of glutamate in the extracellular space (27).…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA NEAT1 promoted IL-6, COX-2, and TNF-a expression by targeting miR-129-5p and activating the Notch signaling pathway in epilepsy (11). LncRNA UCA1 was downregulated in epilepsy, whereas the UCA1/miR-203/MEF2C axis inhibited the activation of NF-kB signaling pathway and IL-6, TNF-a, and Cox-2 levels in epilepsy (12). lncRNA CASC2 suppressed the activation of astrocytes to reduce the frequency of epileptic seizures in epileptic rats, and CASC2 overexpression promoted PTEN expression to inhibit the release of adenosine and astrocyte activation (13).…”

Section: Introductionmentioning

confidence: 96%

Long Noncoding RNA X-Inactive-Specific Transcript Promotes the Secretion of Inflammatory Cytokines in LPS Stimulated Astrocyte Cell Via Sponging miR-29c-3p and Regulating Nuclear Factor of Activated T cell 5 Expression

et al. 2021

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BackgroundAstrocyte activation promotes glutamate accumulation and secretion of inflammatory factors, mainly responsible for epilepsy. Long noncoding RNA (lncRNA) X-inactive-specific transcript (XIST) regulates inflammation; however, the biological role and regulatory mechanism of XIST during astrocyte activation remain unclear.MethodsIn the present study, rat epilepsy model and lipopolysaccharide (LPS)-treated CTX-TNA2 were established. XIST and miR-29c-3p expression were evaluated using quantitative real-time polymerase chain reaction. Nuclear factor of activated T cells 5 (NFAT5) was measured using western blot analysis. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and L-glutamate levels in the culture supernatants were assessed using enzyme-linked immunosorbent assay. The binding between XIST and miR-29c-3p and between miR-29c-3p and the 3′-UTR of NFAT5 was analyzed using dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and Biotin pull-down assay. The proliferation and apoptosis were evaluated using CCK8 and flow cytometry, respectively.ResultsXIST expression and NFAT5 protein level was increased, whereas miR-29c-3p expression was decreased in the epilepsy rat model and LPS-treated CTX-TNA2 cells. Silenced XIST expression, miR-29c-3p overexpression, or silenced NFAT5 expression inhibited the secretion of IL-1β, IL-6, and TNF-α and promoted glutamate transport in LPS-treated CTX-TNA2 cells. miR-29c-3p was the potential miRNA sponged by XIST. NFAT5 acted as a direct binding target of miR-29c-3p. Silenced miR-29c-3p expression or NFAT5 overexpression reversed the effect of silenced XIST expression on LPS-treated CTX-TNA2.XIST and miR-29c-3p treatment does not affect NFAT5 mRNA expression, but affects NFAT5 protein level. Furthermore, underexpressed XIST or overexpressed miR-29c-3p in LPS-stimulated CTX-TNA2 can attenuate neuronal apoptosis induced by LPS-stimulated CTX-TNA2.ConclusionLncRNA XIST promotes the secretion of inflammatory cytokines in LPS- treated CTX-TNA2 via sponging miR-29c-3p and regulating NFAT5 expression.

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“…Unrestricted inflammatory reactions might induct abnormal neuronal bond and hyper-excitable neuronal system, accelerating the initiation and development of epilepsy [3]. The mechanisms of epileptogenesis is deliberated to cover the dysfunction of genes contributing to the progression of neuronal signaling, cell death and inflammation [4].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA NEAT1 aggravates epilepsy and seizure-induced neuronal damage by regulating microRNA-139/ROCK1 axis

Hao

Tao

et al. 2020

Preprint

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Background Both long non-coding RNA (lncRNA) NEAT1 and microRNA (miR)-139 are crucial gene regulators in various disorders. This study aims to investigate their role in epilepsy and seizure-induced neuronal damage. Methods In this research, rat model of epilepsy was established by pilocarpine induction. The RNA and protein expression in hippocampal tissues and neurons were determined by RT-qPCR and Western blot analysis, respectively. Microarray analysis was used to predict the relationship between NEAT1 and miR-139 or between miR-139 and ROCK1, and dual luciferase reporter gene assay was performed to verify the interaction. The endogenous expression of related genes was modulated by recombinant plasmids and cell transfection. The cell apoptosis, levels of inflammatory factors and cell proliferation were detected by flow cytometry, ELISA and EdU assay. Results LncRNA NEAT1 and ROCK1 was upregulated, while the miR-139 was downregulated in hippocampal tissues and neurons of epileptic rats. Overexpression of NEAT1 decreased the activity of neurons, increased cell apoptosis, and increased the level of inflammatory factors. NEAT1 negatively targeted miR-139 to upregulate ROCK1. The RhoA/ROCK1 signaling pathway was activated by NEAT1 overexpression and miR-139 downregulation. Conclusion LncRNA NEAT1 suppressed pilocarpine-induced epilepsy by inhibiting apoptosis of hippocampal neurons through miR-139/RhoA/ROCK1 axis, and thereby inhibiting neuronal injury induced by seizure.

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LncRNA UCA1 Suppresses the Inflammation Via Modulating miR-203-Mediated Regulation of MEF2C/NF-κB Signaling Pathway in Epilepsy

Cited by 39 publications

References 46 publications

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Modulation of TNF-α plasma levels in coronary artery disease [CAD] and non-CAD male patients by lncRNA UCA1 and aspirin

Long Noncoding RNA X-Inactive-Specific Transcript Promotes the Secretion of Inflammatory Cytokines in LPS Stimulated Astrocyte Cell Via Sponging miR-29c-3p and Regulating Nuclear Factor of Activated T cell 5 Expression

Long non-coding RNA NEAT1 aggravates epilepsy and seizure-induced neuronal damage by regulating microRNA-139/ROCK1 axis

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