Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury

Cui, Shengyu; Zhang, Wei; Cui, Zhiming; Yi, Hong; De-sheng, XU; Liu, Wei; Zhu, Xiao Feng

doi:10.1186/s13018-020-02041-6

Cited by 13 publications

(10 citation statements)

References 27 publications

(17 reference statements)

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“…In this review, the lncRNA/circRNA-miRNA-mRNA regulatory network also exists in microglia and astrocyte mediated neurological diseases, including SCI (Figure 1; Shao et al, 2020; FIGURE 1 | The lncRNA/circRNA-miRNA-mRNA regulatory network in microglia and astrocyte regulated neurological diseases. Xu S. et al, 2020;Zhao Q. et al, 2020;Cui et al, 2021;Xiang et al, 2021;Chen et al, 2022), TBI (He et al, 2021;Liu N. et al, 2021;Meng et al, 2021), cerebral IRI (Figure 1; Wang et al, 2020c;Yang et al, 2021), stroke (Figure 1; Qi et al, 2017;Han B. et al, 2018;Tian et al, 2021;Zhang M. et al, 2021), epilepsy (Figure 1; Feng et al, 2020;Han C. L. et al, 2020;Wan and Yang, 2020;Xiaoying et al, 2020), neuropathic pain (Figure 1; Chen M. et al, 2020), PD (Figure 1; Cao et al, 2018Cao et al, , 2021, and depression (Figure 1; . We also found that some therapies can impair the ncRNA-glial cell axis and thus inhibit disease development.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-222-5p can target RAMP3 3 UTR and inhibit RAMP3 expression. Enhanced RAMP3 expression or miR-222-5p inhibitor can promote cell apoptosis and increase TNF-α and IL-6 expressions in LPS-treated microglia (Cui et al, 2021). LncRNA lymphoid enhancer-binding factor 1 (LEF1) antisense RNA 1 (LEF1-AS1) is up-regulated in LPStreated microglia cells that are collected from the central nervous system of normal rats.…”

Section: Spinal Cord Injurymentioning

confidence: 99%

“…Knocking down LEF1-AS1 dampens microglia apoptosis and promotes microglial cell viability through the miR-222-5p-RAMP3 axis. LEF1-AS1 silence can impede SCI progression in rats (Cui et al, 2021). Pyroptosis is a type of programmed cell death involved in neuroinflammation (Dai et al, 2019).…”

Section: Spinal Cord Injurymentioning

confidence: 99%

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Long Non-coding RNAs and Circular RNAs: Insights Into Microglia and Astrocyte Mediated Neurological Diseases

Chen

Lai

Wang

et al. 2021

Front. Mol. Neurosci.

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Microglia and astrocytes maintain tissue homeostasis in the nervous system. Both microglia and astrocytes have pro-inflammatory phenotype and anti-inflammatory phenotype. Activated microglia and activated astrocytes can contribute to several neurological diseases. Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), two groups of non-coding RNAs (ncRNAs), can function as competing endogenous RNAs (ceRNAs) to impair the microRNA (miRNA) inhibition on targeted messenger RNAs (mRNAs). LncRNAs and circRNAs are involved in various neurological disorders. In this review, we summarized that lncRNAs and circRNAs participate in microglia dysfunction, astrocyte dysfunction, neuron damage, and inflammation. Thereby, lncRNAs and circRNAs can positively or negatively regulate neurological diseases, including spinal cord injury (SCI), traumatic brain injury (TBI), ischemia-reperfusion injury (IRI), stroke, neuropathic pain, epilepsy, Parkinson’s disease (PD), multiple sclerosis (MS), and Alzheimer’s disease (AD). Besides, we also found a lncRNA/circRNA-miRNA-mRNA regulatory network in microglia and astrocyte mediated neurological diseases. Through this review, we hope to cast light on the regulatory mechanisms of lncRNAs and circRNAs in microglia and astrocyte mediated neurological diseases and provide new insights for neurological disease treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Spinal Cord Injurymentioning

confidence: 99%

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Long Non-coding RNAs and Circular RNAs: Insights Into Microglia and Astrocyte Mediated Neurological Diseases

Chen

Lai

Wang

et al. 2021

Front. Mol. Neurosci.

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“…The M1 phenotype elicits pro-inflammatory activity with the release of pro-inflammatory factors such as IL-6 and TNF-α, while the M2 phenotype is characteristic of anti-inflammatory activity induced by the release of several anti-inflammatory factors such as IL-10 and TGF-β ( 27 , 28 ). LPS induces activation of M1 microglia ( 28 ), facilitates the apoptosis of microglia, and decreases the cell survival rate ( 29 ). Our results demonstrated that overexpression of miR-124-3p could alleviate the damage of LPS to microglia.…”

Section: Discussionmentioning

confidence: 99%

miR-124-3p Inhibits Microglial Secondary Inflammation After Basal Ganglia Hemorrhage by Targeting TRAF6 and Repressing the Activation of NLRP3 Inflammasome

Fang

Hong

2021

Front. Neurol.

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Objectives: Intracerebral hemorrhage (ICH) represents a serious central nervous system emergency with high morbidity and mortality, and the basal ganglia is the most commonly affected brain region. Differentially expressed microRNAs (miRs) have recently been highlighted to serve as potential diagnostic biomarkers and therapeutic targets for ICH. This study investigated the mechanism of miR-124-3p in microglial secondary inflammation after ICH.Methods: In this study, 48 patients with primary basal ganglia ICH and 48 healthy volunteers were selected and venous blood was collected from all patients on the second morning of admission (within 24 h of stroke onset). The expression of miR-124-3p in serum was detected by RT-qPCR. Three months after ICH, the patients were assessed by modified Rankin Scale (mRS), and the correlation between miR-124-3p expression and mRS score was analyzed by Pearson. The inflammatory response of microglia was induced by lipopolysaccharide (LPS) to establish the cell model of microglial inflammation. miR-124-3p expression patterns were detected in the serum of ICH patients and healthy volunteers, normal microglia, and LPS-induced microglia. The miR-124-3p mimic was transfected into LPS-induced microglia, followed by measurement of the inflammatory factors, apoptosis rate, and cell viability. The target gene of miR-124-3p was predicted and verified. The expression patterns of tumor necrosis factor receptor-associated factor 6 (TRAF6) were detected. pcDNA3.1 and pcDNA3.1-TRAF6 were transfected into LPS-induced HMC3 cells, and nucleotide-binding oligomerization domain-like receptor (NLR) pyrin domain-containing 3 (NLRP3) expression patterns were determined. Lastly, the effects of TRAF6 overexpression on apoptosis, cell viability, and inflammation in HMC3 cells were measured.Results: miR-124-3p was downregulated in the serum of basal ganglia ICH patients and LPS-induced microglia, and miR-124-3p expression was negatively correlated with mRS. Overexpression of miR-124-3p reduced the inflammatory factors and apoptosis rate and promoted cell activity in LPS-induced microglia. miR-124-3p was found to target TRAF6. Overexpression of TRAF6 enhanced the expression of NLRP3 inflammasome, inflammatory factors and apoptosis rate, and reduced cell viability.Conclusion: Our findings indicate that miR-124-3p repressed the activation of NLRP3 inflammasome by targeting TRAF6, thus inhibiting microglial secondary inflammation after ICH in basal ganglia.

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“…In contrast, reductions in SNHG5 decreases the viability of these cells 12. Furthermore, inhibiting the upregulation of the lncRNA LEF1-AS1 after SCI decreases microglial apoptosis and the inflammatory response 13. Recently, we performed a study indicating that many mRNAs are involved in the alleviation of SCI using HBO 14.…”

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confidence: 99%

Hyperbaric Oxygen Treatment in Spinal Cord Injury Recovery: Profiling Long Noncoding RNAs

Liu

Liang

Sun

et al. 2022

Spine

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Study Design. A functional, transcriptome, and long noncoding RNAs (lncRNAs) expression analysis in the spinal cord of mice after hyperbaric oxygen (HBO) treatment. Objective. We aimed to explore the mechanism by which HBO treats spinal cord injury (SCI) at the level of lncRNAs. Summary of Background Data. Immense amounts of research have established that HBO treatment promotes the recovery of neurological function after SCI. The mechanism of action remains to be clarified. Methods. High-throughput RNA sequencing, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were used to profile lncRNA expression and analyze biological function in the spinal cords of mice from sham-operated, SCI, and HBO-treated groups. The differential expression of lncRNA between the groups was assessed using real-time quantitative polymerase chain reaction. Results. Differential expression across 577 lncRNAs was identified among the three groups. GO analysis showed that free ubiquitin chain polymerization, ubiquitin homeostasis, DNA replication, synthesis of RNA primer, single-stranded telomeric DNA binding, and alpha-amylase activity were significantly enriched. Kyoto Encyclopedia of Genes and Genomes enrichment analysis displayed that vitamin B6 metabolism, one carbon pool by folate, DNA replication, lysine degradation, beta-alanine metabolism, fanconi anemia pathway, and Notch signal pathway were the main pathways with enrichment significance. LncRNAs NONMMUT 092674.1, NONMMUT042986.2, and NONMMUT018850.2 showed significantly different expression between the SCI and the other two groups (P<0.05, <0.01). Conclusions. This study is the first to determine the expression profiles of lncRNAs in the injured spinal cord after HBO treatment. We identified several important dysregulated lncRNAs in this setting. These results help us better understand the mechanism by which HBO treats SCI and provide new potential therapeutic targets for SCI.

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Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury

Cited by 13 publications

References 27 publications

Long Non-coding RNAs and Circular RNAs: Insights Into Microglia and Astrocyte Mediated Neurological Diseases

Long Non-coding RNAs and Circular RNAs: Insights Into Microglia and Astrocyte Mediated Neurological Diseases

miR-124-3p Inhibits Microglial Secondary Inflammation After Basal Ganglia Hemorrhage by Targeting TRAF6 and Repressing the Activation of NLRP3 Inflammasome

Hyperbaric Oxygen Treatment in Spinal Cord Injury Recovery: Profiling Long Noncoding RNAs

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