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Hypoxia-ischemia-induced Ntoco promotes ferroptosis via the Hnrnpab-mediated NF κB/Lcn2 axis following traumatic brain injury in mice

ABSTRACT: Hypoxia-ischemia-induced Ntoco promotes ferroptosis via the Hnrnpab-mediated NF κB/Lcn2 axis following traumatic brain injury in mice

PROVIDER: PRJNA986212 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24985100_1.fastq.gz	Fastqsanger.gz
	SRR24985100_2.fastq.gz	Fastqsanger.gz
	SRR24985101_1.fastq.gz	Fastqsanger.gz
	SRR24985101_2.fastq.gz	Fastqsanger.gz
	SRR24985102_1.fastq.gz	Fastqsanger.gz

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Hypoxia-ischemia-induced Ntoco promotes ferroptosis via the Hnrnpab-mediated NF κB/Lcn2 axis following traumatic brain injury in mice

Project description:Evidence supports the contribution of long non-coding RNAs (lncRNAs) and ferroptosis to traumatic brain injury (TBI) pathogenesis. However, lncRNA regulation in TBI-induced ferroptosis remains poorly understood. Herein, we identified an lncRNA, named noncoding transcript of chemokine (C-C motif) ligand 4 (Ccl4) overlapping (Ntoco), which was upregulated in TBI mice. The upregulation was initiated by hypoxia ischemia induced lower enrichment of H3K27me3 on the Ntoco promoter. Ntoco knockdown inhibited neuron ferroptosis, ameliorated spatial memory and lesion volume following TBI. Ntoco overexpression promoted neuron ferroptosis and recruited microglia to provoke an inflammatory response via Ccl4. Mechanistically, Ntoco facilitated K48-linked ubiquitination and protein degradation by binding to Hnrnpab, which suppressed NF-κB/Lcn2 signal axis activation, including decreased phosphorylation of IkBα, increased phosphorylation of IKKα/β, nuclear translocation of the NF-κB p65 subunit, and elevated Lcn2 expression. These data indicated that targeting Ntoco to mitigate ferroptosis might be a potential therapeutic strategy for TBI.

2024-06-21 | GSE235523 | GEO

Ntoco Promotes Ferroptosis via Hnrnpab-Mediated NF-κB/Lcn2 Axis Following Traumatic Brain Injury in Mice.

Project description:ObjectiveEmerging evidence highlights the involvement of long non-coding RNAs (lncRNAs) and ferroptosis in the pathogenesis of traumatic brain injury (TBI). However, the regulatory role of lncRNAs in TBI-induced ferroptosis remains poorly understood. This study aims to investigate the role of a specific lncRNA, noncoding transcript of chemokine (C-C motif) ligand 4 (Ccl4) overlapping (Ntoco), in the regulation of ferroptosis following TBI and explore its potential as a therapeutic target.MethodsThe expression levels of Ntoco following controlled cortical injury (CCI) in mice were measured using real-time PCR. Behavioral tests post-injury were assessed using the rotarod test and Morris water maze, and lesion volume was evaluated using micro-MRI. Ntoco binding proteins were identified using RNA pull-down and RNA immunoprecipitation. RNA sequencing was employed to identify Ntoco-related pathways. Western blotting and co-immunoprecipitation were used to measure protein levels and ubiquitination processes.ResultsNtoco upregulation was observed in CCI mice. Ntoco knockdown inhibited neuron ferroptosis, reduced lesion volume, and improved spatial memory following TBI. Ntoco overexpression promoted ferroptosis in neurons. Mechanistically, Ntoco facilitated K48-linked ubiquitination and degradation of proteins by binding to Hnrnpab, suppressing the NF-κB/Lcn2 signaling pathway. This included reduced phosphorylation of IkBα, increased phosphorylation of IKKα/β, nuclear translocation of the NF-κB p65 subunit, and elevated Lcn2 expression.ConclusionOur findings suggest that Ntoco plays a crucial role in TBI-induced ferroptosis by modulating the NF-κB/Lcn2 signaling pathway. Targeting Ntoco may provide a promising therapeutic strategy to mitigate ferroptosis and improve outcomes following TBI.

| S-EPMC11840698 | biostudies-literature

LncRNA regulated by hnRNPAB in HCC cell lines

Project description:To reveal the HNRNPAB-regulated lncRNAs, we performed microarray analyses to screen differential lncRNAs in HCC cells after stable overexpression or knockdown of HNRNPAB. MHCC97H and HCCLM3 (HCC cell lines with high-metastatic potentials), PLC/PRF/5 and HepG2 (HCC cell lines with low-metastatic potentials) were used in this study. HepG2-control, HepG2-hnRNPAB, PLC/PRF/5-control, PLC/PRF/5-hnRNPAB, MHCC97H-control, MHCC97H-sh-hnRNPAB, HCCLM3-control, HCCLM3-sh-hnRNPAB were perpared with hU6-MCS-CBh-gcGFP-IRES-puromycin-shRNA-HNRNPAB/mock lentiviral and Ubi-MCS-SV40-EGFP-IRES-puromycin-HNRNPAB/mock cDNA lentiviral,respectively, each performed in triplicate.

2019-01-01 | GSE124516 | GEO

RNA-seq of HNRNPAB morpholino in zebrafish

Project description:To investigate the transcriptomic alterations following 24hpf knockdown of the gene HNRNPAB in zebrafish, we injected HNRNPAB morpholino with 3ng and 6ng into 1-cell zebrafish embryos separately, and the 24hpf embryos were collected for RNA-seq.

2022-03-31 | GSE199586 | GEO

Inhibiting LCN2 can suppress the development of NSCLC by promoting ferroptosis

Project description:Ferroptosis, a recently discovered form of regulated cell death, has been closely linked to tumor progression. However, the underlying mechanism of ferroptosis in non-small cell lung cancer (NSCLC) remains unclear. In this study, we conducted transcriptome sequencing on NSCLC samples. Overall, our study suggests that suppressing LCN2 can effectively inhibit the development of NSCLC by promoting ferroptosis

2023-07-27 | GSE238161 | GEO

Mouse primary astrocytes: LCN2 protein treated vs. control

Project description:Transcriptional profiling of mouse primary astrocytes comparing control untreated astrocytes with astrocytes treated with recombinant LCN2 protein (10 micro gram/ml). Goal was to determine the effects of LCN2 treatment on global gene expression in astrocytes. A secreted protein lipocalin-2 (LCN2) has been implicated in diverse cellular processes including cell morphology and migration. We have previously demonstrated that lcn2 mediates reactive astrocytosis. In order to further understand the role of lcn2 in the CNS, astrocyte transcriptome was analyzed following LCN2 treatment. Chemokines were the major group of genes upregulated by LCN2. Two-condition experiment, control untreated astrocytes vs. LCN2 protein treated astrocytes. Biological replicates: 1 control replicates, 1 treated replicates.

2012-06-29 | E-GEOD-15667 | biostudies-arrayexpress

Mouse primary astrocytes: LCN2 protein treated vs. control

2012-06-30 | GSE15667 | GEO

A targetable LIFR-NF-κB-LCN2 axis controls liver tumorigenesis and vulnerability to ferroptosis.

Project description:The growing knowledge of ferroptosis has suggested the role and therapeutic potential of ferroptosis in cancer, but has not been translated into effective therapy. Liver cancer, primarily hepatocellular carcinoma (HCC), is highly lethal with limited treatment options. LIFR is frequently downregulated in HCC. Here, by studying hepatocyte-specific and inducible Lifr-knockout mice, we show that loss of Lifr promotes liver tumorigenesis and confers resistance to drug-induced ferroptosis. Mechanistically, loss of LIFR activates NF-κB signaling through SHP1, leading to upregulation of the iron-sequestering cytokine LCN2, which depletes iron and renders insensitivity to ferroptosis inducers. Notably, an LCN2-neutralizing antibody enhances the ferroptosis-inducing and anticancer effects of sorafenib on HCC patient-derived xenograft tumors with low LIFR expression and high LCN2 expression. Thus, anti-LCN2 therapy is a promising way to improve liver cancer treatment by targeting ferroptosis.

| S-EPMC8683481 | biostudies-literature

RNA-seq of HNRNPAB morpholino in zebrafish

Project description:RNA-seq of HNRNPAB morpholino in zebrafish

| PRJNA820769 | ENA

Gene expression analysis in proximal and distal colons of Lcn2-/- IL10-/- double knock-out mice.

Project description:Lcn2 is involved in host defense against pathogens, but the function in intestinal mucosal immunity and inflammation remains largely unknown. Genetic ablation of Lcn2 results in early-onset colitis and spontaneous emergence of right-sided colonic tumors in the setting of IL-10 deficiency (Lcn2-/-;IL10-/- mice). To address whether inflammation or other mechanisms drives the site-specific tumor locations gene expression analyses in proximal versus distal colons of Lcn2-/- IL10-/- mice were performed. Differential expression between distal colon versus cecum and proximal colon samples were analyses using Affymetrix MoGene 2.0 ST arrays on formalin-fixed, paraffin-embedded tissue sections of Lcn2-/-; IL10-/-mice.

2016-03-30 | E-MTAB-4583 | biostudies-arrayexpress

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