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Survival Following Traumatic Brain Injury in Drosophila Is Increased by Heterozygosity for a Mutation of the NF-κB Innate Immune Response Transcription Factor Relish

ABSTRACT: Survival Following Traumatic Brain Injury in Drosophila Is Increased by Heterozygosity for a Mutation of the NF-κB Innate Immune Response Transcription Factor Relish

PROVIDER: PRJNA660065 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12544400_1.fastq.gz	Fastqsanger.gz
	SRR12544400_2.fastq.gz	Fastqsanger.gz
	SRR12544401_1.fastq.gz	Fastqsanger.gz
	SRR12544401_2.fastq.gz	Fastqsanger.gz
	SRR12544402_1.fastq.gz	Fastqsanger.gz

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NF-κB activation in astrocytes critically affects wound regeneration after traumatic brain injury

Project description:Traumatic brain injury (TBI) is a complex condition in which multiple pathophysiological mechanisms influence the course of the disease. After the primary mechanical impact, neuroinflammatory reactions of glial cells along with infiltrating peripheral immune cells mainly determine the overall clinical outcome. However, these secondary processes and their molecular determinants promoting either beneficial or detrimental consequences are not well-defined. Here, we show that TBI-mediated NF-κB activation in astrocytes impairs their homeostatic functions and acts as a key regulator of multiple post-traumatic responses in mice. We determined striking deficits in CNS scar formation after TBI using a combination of NF-κB-reporter mice, conditional mouse models allowing astrocytic NF-κB modulation, and analysis of transcriptomic signatures. Importantly, the development of wound healing deficits depends on paracrine signaling of NF-κB-activated astrocytes and cross-responsive microglial cells. Our findings identify astrocytic NF-κB activation as a critical pathological amplification factor interfering with the restoration of CNS integrity at wound lesion sites.

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NF-κB activation in astrocytes critically affects wound regeneration after traumatic brain injury II

Project description:Traumatic brain injury (TBI) is a complex condition in which multiple pathophysiological mechanisms influence the course of the disease. After the primary mechanical impact, neuroinflammatory reactions of glial cells along with infiltrating peripheral immune cells mainly determine the overall clinical outcome. However, these secondary processes and their molecular determinants promoting either beneficial or detrimental consequences are not well-defined. Here, we show that TBI-mediated NF-κB activation in astrocytes impairs their homeostatic functions and acts as a key regulator of multiple post-traumatic responses in mice. We determined striking deficits in CNS scar formation after TBI using a combination of NF-κB-reporter mice, conditional mouse models allowing astrocytic NF-κB modulation, and analysis of transcriptomic signatures. Importantly, the development of wound healing deficits depends on paracrine signaling of NF-κB-activated astrocytes and cross-responsive microglial cells.Our findings identify astrocytic NF-κB activation as a critical pathological amplification factor interfering with the restoration of CNS integrity at wound lesion sites.

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Survival Following Traumatic Brain Injury in Drosophila Is Increased by Heterozygosity for a Mutation of the NF-κB Innate Immune Response Transcription Factor Relish

Project description:To identify genes regulated by Relish in both the absence and presence of TBI in Drosophila, we compared genome-wide mRNA expression of control flies, as well as flies that were heterozygous or homozygous for a null allele of relish with and without injury.

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Insect hormone prothoracicotropic hormone (PTTH) regulates lifespan through temporal and spatial activation of NF-κB signaling during Drosophila metamorphosis [1]

Project description:The prothoracicotropic hormone (PTTH) is a well-known neuropeptide that regulates insect metamorphosis (the juvenile-to-adult transition) by inducing the biosynthesis of steroid hormones, similar to the hypothalamic-pituitary-gonadal control of mammalian puberty. However, the role of Ptth in adult physiology and longevity is largely unexplored. Here, we show that Ptth loss-of-function mutants are long-lived and exhibit increased resistance to oxidative stress in Drosophila. Intriguingly, we find that loss of Ptth blunt age-dependent upregulation of NF-κB signaling specifically in fly oenocytes, the homolog of mammalian hepatocytes. We further show that oenocyte-specific overexpression of NF-κB/Relish blocks the lifespan extension of Ptth mutants, suggesting that Ptth regulates lifespan through oenocyte-specific NF-κB signaling. Surprisingly, adult-specific knockdown of Ptth did not prolong lifespan, indicating that Ptth might control longevity through developmental programs. Our developmental transcriptomic analysis reveals an interesting activation of NF-κB signaling during fly metamorphosis, which is attenuated in Ptth mutants. Intriguingly, the knockdown of NF-κB/Relish, specifically in oenocytes during metamorphosis, significantly prolongs the lifespan of adult flies. Thus, our findings uncover an unexpected role of insect hormone PTTH in controlling adult lifespan through temporal and spatial activation of NF-κB signaling in developing hepatocytes.

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Insect hormone prothoracicotropic hormone (PTTH) regulates lifespan through temporal and spatial activation of NF-κB signaling during Drosophila metamorphosis [2]

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NF-κB activation in astrocytes critically affects wound regeneration after traumatic brain injury

Project description:NF-κB activation in astrocytes critically affects wound regeneration after traumatic brain injury

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2024-02-28 | PXD040125 | Pride

NF-κB activation in astrocytes critically affects wound regeneration after traumatic brain injury II

Project description:NF-κB activation in astrocytes critically affects wound regeneration after traumatic brain injury II

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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.

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