circ-Ncam2 (mmu_circ_0006413) Participates in LPS-Induced Microglia Activation and Neuronal Apoptosis via the TLR4/NF-κB Pathway

Guo, Kai; Chang, Yunlong; Jin, Yutao; Yan, Hong; Che, Ping

doi:10.1007/s12031-022-02018-6

Cited by 7 publications

(7 citation statements)

References 37 publications

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“…CircRNA can be involved in the regulation of a variety of diseases such as cancer, cardiovascular diseases, and nervous system diseases [30]. CircRNAs including circ _014301 [31], circ_Hecw1 [32], circ_Ncam2 [33], and circ_0004381 [34] were also reported to be involved in LPS-induced neuroinflammation, which may participate in the pathogenesis of AD. Xie et al reported that circRNA_014301 could silence alleviated apoptosis and inflammation in PC12 cells [31].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the expression of circ Hecw1 in LPS-triggered PC12 cells was significantly decreased [32]. Furthermore, researchers have shown that the circ-Ncam2 [33] and circ_0004381 [34] were upregulated in LPS-induced microglia activation. In the present study, we have detected four DEcircRNAs between the LPS-induced AD mice model and AD mice model treated with BM25, which may indicate these circRNAs were involved in the pathogenesis of AD treated with BM25.…”

Section: Discussionmentioning

confidence: 99%

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In-depth analyses of lncRNA and circRNA expression in the hippocampus of LPS-induced AD mice by Byu d Mar 25

Zhang,

Tang,

Wang

et al. 2023

NeuroReport

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Byu d Mar 25 (BM25) has been verified to have neuroprotective effects in Alzheimer’s disease (AD) mice. However, the molecular mechanism remains unclear. We aimed to investigate the expression profiling of lncRNAs and circRNAs by microarray analysis. Six hippocampus from LPS-mediated AD mice model treated with (normal saline (NS) (n = 3) and AD mice model treated with BM25 (n = 3) were selected. Microarray analysis was performed to detect the expression profiles of lncRNAs and circRNAs in hippocampus. Differentially expressed (DE) lncRNAs, mRNAs and circRNAs were identified through scatter plot and volcano plot filtering with a threshold of fold-change ≥2 and P ≤ 0.05. Co-expression network is analyzed by Circos software. Cis- and Trans- regulation were analyzed using RIsearch-2.0 and FEELNC softwares. LncRNA-transcription factors (TFs) and LncRNA-Target-TFs network were analyzed by Clusterprofiler software. The prediction of miRNAs bind to circRNAs were performed with miRNAbase. A total of 113 DElncRNAs, 117 DEmRNAs, and 4 DEcircRNAs were detected. The pathway analysis showed the mRNAs that correlated with lncRNAs were involved in apoptosis, inflammatory mediator regulation of TRP channels, NF-kappa B and PI3K-Akt signaling pathway. The lncRNA-TFs network analysis suggested the lncRNAs were mostly regulated by Ncoa1, Phf5a, Klf6, Lmx1b, and Pax3. Additionally, lncRNA-target-TFs network analysis indicated the GATA6, Junb, Smad1, Twist1, and Mafb mostly regulate the same lncRNAs: XR_001783430.1 and NR_051982.1. Furthermore, 480 miRNAs were predicted binding to 4 identified circRNAs. The BM25 may affect AD by regulating the expression of lncRNAs and circRNAs, which could regulate the expressions of mRNAs or miRNAs by LncRNA-Target-TFs network.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

In-depth analyses of lncRNA and circRNA expression in the hippocampus of LPS-induced AD mice by Byu d Mar 25

Zhang,

Tang,

Wang

et al. 2023

NeuroReport

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“…PC12 cell culture and treatment. LPS can induce inflammation in Pc12 cells via Tlr4 activity and it is widely used for Sci model in vitro (24)(25)(26). in the present study, the Pc12 cells induced by lPS was used for the Sci model in vitro.…”

Section: Euthanasia Of Experimental Animals and Sample Handlingmentioning

confidence: 97%

S100A1 expression is increased in spinal cord injury and promotes inflammation, oxidative stress and apoptosis of PC12 cells induced by LPS via ERK signaling

Bai

Guo²,

Xu³

et al. 2022

Mol Med Rep

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Spinal cord injury (Sci) is a severe neurological disorder and the molecular mechanisms leading to its poor prognosis remain to be elucidated. S100a1, a mediator of ca 2+ handling of sarcoplasmic reticulum and mitochondrial function, operates as an endogenous danger signal (alarmin) associated with inflammatory response and tissue injury. The aim of the present study was to investigate the expression and biological effects of S100a1 in Sci. a rat model of Sci and a Pc12 cell model of lipopolysaccharide (lPS)-induced inflammation were established to examine S100a1 expression at the mrna and protein levels. The inflammation level, which was mediated by S100A1, was determined based on inflammatory factor (il-1β, il-6 and TnF-α) and anti-inflammatory factor (IL-10) expression. The effects of S100a1 on cellular oxidation and anti-oxidation levels were observed by detecting the levels of reactive oxygen species, superoxide dismutase, catalase activities and nuclear factor erythroid 2-related factor 2 expression. The protein levels of Bax, Bcl2 and cleaved caspase-3 were used for the evaluation of the effects of S100a1 on apoptosis. Phosphorylated (p-)erK1/2 expression was used to evaluate the effects of S100a1 on erK signaling. The results revealed that S100A1 expression was significantly upregulated in vivo and in vitro in the PC12 cell model of LPS-inflammation. The silencing and overexpression of S100a1 helped alleviate and aggravate LPS-induced inflammation, oxidative stress and apoptosis levels, respectively. S100a1 was found to regulate the erK signaling pathway positively. an inhibitor of erK signaling (MK-8353) partially abolished the promoting effects of the overexpression of S100A1 on inflammation, oxidative stress damage and apoptosis. in conclusion, S100a1 expression was elevated in model of Sci and in the Pc12 cell model of LPS-induced inflammation. Furthermore, the overexpression/silencing S100A1 aggravated/mitigated the inflammation, oxidative stress damage and the apoptosis of lPS-stimulated Pc12 cells via the erK signaling pathway. The present study revealed the mechanism of S100a1 in Sci, which provided a new theoretic reference for future research on Sci.

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“… 124 Silencing of circ-Ncam2 induced miR-544-3p expression, which inhibited activation of the TLR4/NF-κB pathway, reduced activation of LPS-treated microglia, and inhibited neuronal apoptosis, thereby promoting recovery from SCI. 125 …”

Section: Roles Of Mirnas In Macrophage-mediated Inflammationmentioning

confidence: 99%

Non-Coding RNAs Regulate Spinal Cord Injury-Related Neuropathic Pain via Neuroinflammation

Huang¹,

Hu²,

Qiao³

et al. 2023

JIR

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Secondary chronic neuropathic pain (NP) in addition to sensory, motor, or autonomic dysfunction can significantly reduce quality of life after spinal cord injury (SCI). The mechanisms of SCI-related NP have been studied in clinical trials and with the use of experimental models. However, in developing new treatment strategies for SCI patients, NP poses new challenges. The inflammatory response following SCI promotes the development of NP. Previous studies suggest that reducing neuroinflammation following SCI can improve NP-related behaviors. Intensive studies of the roles of non-coding RNAs in SCI have discovered that ncRNAs bind target mRNA, act between activated glia, neuronal cells, or other immunocytes, regulate gene expression, inhibit inflammation, and influence the prognosis of NP.

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circ-Ncam2 (mmu_circ_0006413) Participates in LPS-Induced Microglia Activation and Neuronal Apoptosis via the TLR4/NF-κB Pathway

Cited by 7 publications

References 37 publications

In-depth analyses of lncRNA and circRNA expression in the hippocampus of LPS-induced AD mice by Byu d Mar 25

In-depth analyses of lncRNA and circRNA expression in the hippocampus of LPS-induced AD mice by Byu d Mar 25

S100A1 expression is increased in spinal cord injury and promotes inflammation, oxidative stress and apoptosis of PC12 cells induced by LPS via ERK signaling

Non-Coding RNAs Regulate Spinal Cord Injury-Related Neuropathic Pain via Neuroinflammation

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