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Complement factor C1q mediates sleep spindle disruption and epileptic spikes after mild brain injury

ABSTRACT: Complement factor C1q mediates sleep spindle disruption and epileptic spikes after mild brain injury

PROVIDER: PRJNA744171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15050665_1.fastq.gz	Fastqsanger.gz
	SRR15050665_2.fastq.gz	Fastqsanger.gz
	SRR15050666_1.fastq.gz	Fastqsanger.gz
	SRR15050666_2.fastq.gz	Fastqsanger.gz
	SRR15050667_1.fastq.gz	Fastqsanger.gz

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Complement factor C1q mediates sleep spindle disruption and epileptic spikes after mild brain injury

Project description:While traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of mild cortical injury that does not directly damage subcortical structures (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic circuit. Increased C1q expression co-localized with neuron loss and chronic inflammation, and correlated with disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are the source of thalamic C1q. Since the corticothalamic circuit is important for cognition and sleep, which can be impaired by TBI, this circuit could thus be a new target for treating TBI-related disabilities.

2021-09-14 | GSE179541 | GEO

Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury.

Project description:Although traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of mild TBI (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic system. Increased C1q expression colocalized with neuron loss and chronic inflammation and correlated with disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are a source of thalamic C1q. The corticothalamic circuit could thus be a new target for treating TBI-related disabilities.

| S-EPMC8750918 | biostudies-literature

Regulation of neuronal gene and miRNA expression by the complement protein C1q associated with neuroprotection

Project description:Identification of transcriptional profiles stimulated by the complement protein C1q in rat immature neurons associated with the C1q-dependent neuroprotection observed in vitro. Use of the unbiased whole genome microarray approach to identify genes regulated by C1q. Immature neurons grown in vitro for 3 days were stimulated with 10 nM C1q for 3h.

2011-03-07 | E-GEOD-18860 | biostudies-arrayexpress

Regulation of neuronal gene and miRNA expression by the complement protein C1q associated with neuroprotection

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Modulation of gene expression by complement protein C1q in amyloid-beta injured neurons

Project description:Complement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection. Immature rat cortical primary neurons are treated with fibrillar amyloid-beta peptides and/or C1q for 3h before RNA extraction and hybridization on rat Affymetrix microarrays. Supplementary file: Processed/normalized, probe-level signal intensities from neurons treated with amyloid-beta or C1q. Median signal intensity used as global normalization method, done with JMP genomics (v5.0) software.

2012-12-21 | E-GEOD-28886 | biostudies-arrayexpress

Modulation of gene expression by complement protein C1q in amyloid-beta injured neurons

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Project description:spikes

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C1q reprograms innate immune memory [ChIP-seq]

Project description:Innate immune memory, also called trained immunity, is a metabolic and epigenetically regulated process that enables innate immune cells to recalibrate their inflammatory reactivity in response to pathogenic or endogenous stimuli. In addition to its function in host defense, trained immunity contributes to diverse immune-mediated diseases. We discovered that complement component 1q (C1q) is an effective modulator of innate immune memory, potently suppressing the responsiveness of myeloid cells. We found that C1q leads to profound reprogramming of myeloid cell metabolism, particularly glycolysis, and exerts control over the transcriptional regulation of important metabolic and inflammatory genes. We corroborate our findings by identifying single-nucleotide polymorphisms close to the C1q gene that are linked to induction of trained immunity in healthy volunteers. Our results reveal a novel immunomodulatory role for C1q and provide evidence of a molecular interaction between the complement system and innate immune memory. These findings expand our understanding of innate immune memory and provide a promising new target for therapeutic intervention.

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C1q reprograms innate immune memory [RNA-seq]

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