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Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience III

ABSTRACT: Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience III

PROVIDER: PRJNA940107 | ENA |

REPOSITORIES: ENA

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	SRR23675114.fastq.gz	Fastqsanger.gz
	SRR23675115.fastq.gz	Fastqsanger.gz
	SRR23675116.fastq.gz	Fastqsanger.gz
	SRR23675117.fastq.gz	Fastqsanger.gz

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Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience

Project description:Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience

| PRJNA940101 | ENA

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience II

Project description:Here we report that activation of cyclic GMP-AMP synthase (cGAS) diminishes cognitive resilience by decreasing the neuronal transcriptional network of myocyte enhancer factor 2c (MEF2C) through type I interferon (IFN-I) signaling. Pathogenic tau activates cGAS and IFN-I responses in microglia, in part mediated by cytosolic leakage of mitochondrial DNA. Genetic ablation of cGAS in tauopathy mice diminished microglial IFN-I response, preserved synapse integrity and plasticity, and protected against cognitive impairment without affecting the pathogenic tau load. cGAS ablation enhanced, while activation of IFN-I downregulated, neuronal MEF2C expression network linked with cognitive resilience in AD.

2023-04-26 | GSE226381 | GEO

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience II

Project description:Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience II

| PRJNA940108 | ENA

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience I

Project description:Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience I

| PRJNA940104 | ENA

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience IV

Project description:Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience IV

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Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience IV

Project description:Pharmacological inhibition of cGAS with TDI-6570 protected against the synaptic loss and cognitive deficits in P301S tauopathy model, likely via enhancing MEF2C transcriptional network and associated cognitive resilience

2023-04-26 | GSE226383 | GEO

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience III

Project description:To induce chronic IFN-I activation, we injected wildtype and Ifnar1–/– mice with five treatments of DMXAA, a STING agonist, followed by snRNA-seq analysis of hippocampal tissues. In wildtype mice, we showed that microglia had the strongest IFN response to STING activation of all cell types. Ablation of interferon alpha and beta receptor 1 (IFNAR1) abolished microglial IFN-I response and suppression of neuronal MEF2C transcriptional network

2023-04-26 | GSE226382 | GEO

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-04-26 | GSE226385 | GEO

Cyclic GMP-AMP synthase and interferon activation diminish MEF2C-mediated cognitive resilience I

Project description:Analysis of differentially expressed genes (DEGs) revealed a striking upregulation of interferon genes in P301S, compared to non-transgenic hippocampi, and enrichment of transcription factor motifs of interferon-response factors (IRFs) and interferon-sensitive response elements (ISREs). Cgas deletion reduced the induction of a subset of tau-stimulated inflammatory and cytokine expression including interferon stimulated genes such as Stat1, Ddx60, Isg20, Rnf213, Parp12, Ifi35, and Sp100. Thus, microglial cGAS promotes IFN-I expression in response to tau.

2023-04-26 | GSE226380 | GEO

Cyclic GMP–AMP Synthase (cGAS) Deletion Reduces Severity in Bilateral Nephrectomy Mice through Changes in Neutrophil Extracellular Traps and Mitochondrial Respiration

Project description:Uremia-induced systemic inflammation is partly caused by the dissemination of microbial molecules such as lipopolysaccharide and bacterial double-stranded DNA from leaked gut damaged by immune cells in response to the microbial molecules. Cyclic GMP–AMP synthase (cGAS) can recognize fragmented DNA and induce cGAMP synthesis for the activation of the stimulator of interferon genes (STING) pathway. To study the effect of cGAS in uremia-induced systemic inflammation, we performed bilateral nephrectomy (BNx) in wild-type and cGAS knock-out mice and found that the gut leakage and blood uremia from both groups were similar. However, serum cytokines (TNF-α and IL-6) and neutrophil extracellular traps (NETs) decreased significantly in cGAS-/- neutrophils after stimulation with LPS or bacterial cell-free DNA. Transcriptomic analysis of LPS-stimulated cGAS-/- neutrophils also confirmed the down-regulation of neutrophil effector functions. The extracellular flux analysis showed that cGAS-/- neutrophils exhibited a higher respiratory rate than wild-type neutrophils despite having similar mitochondrial abundance and function. Our results suggest that cGAS may control effector functions and the mitochondrial respiration of neutrophils in response to LPS or bacterial DNA.

2023-04-20 | GSE220693 | GEO

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