Long non-coding RNA Peg13 attenuates the sevoflurane toxicity against neural stem cells by sponging microRNA-128-3p to preserve Sox13 expression

Wang, Yue; Sun, Yinghao; Jiang, Hong

doi:10.1371/journal.pone.0243644

Cited by 22 publications

(10 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5 A). Our observation is consistent with previously published results regarding Peg13 localization in neural stem cells ( Jiang et al 2020 ). Next, we tested whether knockdown of Peg13 in iNs would result in a loss of imprinted expression of the surrounding protein-coding genes.…”

Section: Resultssupporting

confidence: 94%

Allelic chromatin structure precedes imprinted expression ofKcnk9during neurogenesis

Loftus,

Bae,

Whilden

et al. 2023

Genes Dev.

View full text Add to dashboard Cite

Differences in chromatin state inherited from the parental gametes influence the regulation of maternal and paternal alleles in offspring. This phenomenon, known as genomic imprinting, results in genes preferentially transcribed from one parental allele. While local epigenetic factors such as DNA methylation are known to be important for the establishment of imprinted gene expression, less is known about the mechanisms by which differentially methylated regions (DMRs) lead to differences in allelic expression across broad stretches of chromatin. Allele-specific higher-order chromatin structure has been observed at multiple imprinted loci, consistent with the observation of allelic binding of the chromatin-organizing factor CTCF at multiple DMRs. However, whether allelic chromatin structure impacts allelic gene expression is not known for most imprinted loci. Here we characterize the mechanisms underlying brain-specific imprinted expression of thePeg13-Kcnk9locus, an imprinted region associated with intellectual disability. We performed region capture Hi-C on mouse brains from reciprocal hybrid crosses and found imprinted higher-order chromatin structure caused by the allelic binding of CTCF to thePeg13DMR. Using an in vitro neuron differentiation system, we showed that imprinted chromatin structure precedes imprinted expression at the locus. Additionally, activation of a distal enhancer induced imprinted expression ofKcnk9in an allelic chromatin structure-dependent manner. This work provides a high-resolution map of imprinted chromatin structure and demonstrates that chromatin state established in early development can promote imprinted expression upon differentiation.

show abstract

Section: Resultssupporting

confidence: 94%

Allelic chromatin structure precedes imprinted expression ofKcnk9during neurogenesis

Loftus,

Bae,

Whilden

et al. 2023

Genes Dev.

View full text Add to dashboard Cite

show abstract

“…Thus, we speculated that AdipoAI might regulate the secretion of cytokines through the coexpression network. Among the network, lncRNA Peg13 regulates the Wnt/β-catenin pathway through the mir-490-3p/psmd11 axis ( 50 ) and attenuates the toxicity of sevoflurane to neural stem cells through the absorption of mir-128-3p while protecting the expression of SOX13 ( 51 ). At the same time, Peg13 can also alleviate hypoxic-ischaemic brain injury in neonatal mice via the mir-20a-5p/XIAP axis ( 52 ).…”

Section: Discussionmentioning

confidence: 99%

Construction of ceRNA and m6A-related lncRNA networks associated with anti-inflammation of AdipoAI

Huang²,

Xie³

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

BackgroundAdiponectin (APN) is an endogenous adipokine secreted from adipocytes that exerts anti-inflammatory properties. AdipoAI is an orally active adiponectin receptor agonist identified by our group that can emulate APN's anti-inflammatory properties through mechanisms that are not fully understood. LncRNAs, a type of noncoding RNA more than 200 bp in length, have been demonstrated to have abundant biological functions, including in anti-inflammatory responses.Materials and ResultIn the current study, we performed a lncRNA microarray in LPS-induced Raw264.7 cells that were prestimulated with AdipoAI and screened 110 DElncRNAs and 190 DEmRNAs. Enrichment analyses were conducted on total mRNAs and DEmRNAs, including GSVA, ssGSEA, GO/KEGG, GSEA, and PPI analysis. Among all these processes, endocytosis was significantly enriched. A coexpression analysis was built based on DElncRNAs and DEmRNAs. Then, using TargetScan and miRwalk to predict related microRNAs of DElncRNAs and DEmRNAs, respectively, we established competing endogenous RNA (ceRNA) networks including 54 mRNAs from 8 GO items. Furthermore, 33 m6A methylation-related marker genes were obtained from a previous study and used for the construction of an m6A-related lncRNA network by coexpression analysis. We identified FTO as the hub gene of the network and 14 lncRNAs that interacted with it. The expression levels of 10 lncRNAs selected from ceRNA and FTO-related lncRNA networks were validated with qRT‒PCR. Finally, macrophage phenotype scores showed that AdipoAI could attenuate the M2b and M2c polarization of macrophages and correlate with the above lncRNAs.ConclusionOur work reveals that lncRNAs might be involved in the anti-inflammation process of AdipoAI in LPS-induced macrophages through the ceRNA network and the epigenetic regulation of m6A. Mechanistically, these lncRNAs associated with AdipoAI might be related to endocytosis and polarization in macrophages and provide new candidates for the anti-inflammatory application of APN and its receptor agonist.

show abstract

“…As is well known, lncRNAs are related to many biological processes during development (such as neuronal development, plasticity, disease, and evolution) and are related with sevoflurane [ 19 , 20 ]. For example, overexpression of Gm15621 [ 21 ] or knockdown of Gm43050 [ 22 ] both attenuates sevoflurane-induced neuronal apoptosis and inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Effects of lncRNA HOXA11-AS on Sevoflurane-Induced Neuronal Apoptosis and Inflammatory Responses by Regulating miR-98-5p/EphA4

Wang

Chen

et al. 2023

Mediators of Inflammation

View full text Add to dashboard Cite

Objective. To explore the molecular mechanism of sevoflurane-induced neurotoxicity and to determine whether lncRNA HOXA11-AS affects sevoflurane-induced neuronal apoptosis and inflammation by regulating miR-98-5p/EphA4. Methods. Morris water maze (MWM) test was used to detect the learning and memory ability of rats, HE staining was used to observe hippocampal pathology, TUNEL staining was used to detect the level of neuronal apoptosis, and RT-qPCR was used to detect the expression of HOXA11-AS, miR-98-5p, IL-6, IL-1β, and TNF-α. At the same time, the contents of IL-6, IL-1β, and TNF-α in serum were detected by ELISA. The expressions of apoptosis-related proteins EphA4, Bax, Cleaved caspase 3, and Bcl-2 were detected by Western blot. The dual-luciferase gene reporter verified the targeting relationship between HOXA11-AS and miR-98-5p and the targeting relationship between miR-98-5p and EphA4. Results. The expression of HOXA11-AS was observed in sevoflurane-treated rats or cells and promoted neuronal apoptosis and inflammation. HOXA11-AS was knocked out alone, or miR-98-5p was overexpressed which attenuates neuronal apoptosis and inflammatory inflammation after sevoflurane treatment. Furthermore, knockdown of HOXA11-AS alone was partially restored by knockdown of miR-98-5p or overexpression of EphA4. Conclusion. Inhibition of lncRNA HOXA11-AS attenuates sevoflurane-induced neuronal apoptosis and inflammatory responses via miR-98-5p/EphA4.

show abstract

Long non-coding RNA Peg13 attenuates the sevoflurane toxicity against neural stem cells by sponging microRNA-128-3p to preserve Sox13 expression

Cited by 22 publications

References 46 publications

Allelic chromatin structure precedes imprinted expression ofKcnk9during neurogenesis

Allelic chromatin structure precedes imprinted expression ofKcnk9during neurogenesis

Construction of ceRNA and m6A-related lncRNA networks associated with anti-inflammation of AdipoAI

Effects of lncRNA HOXA11-AS on Sevoflurane-Induced Neuronal Apoptosis and Inflammatory Responses by Regulating miR-98-5p/EphA4

Contact Info

Product

Resources

About