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Single-cell sequencing of cortical cells following murine traumatic brain injury [scRNA-seq]

ABSTRACT: Single-cell sequencing of cortical cells following murine traumatic brain injury [scRNA-seq]

PROVIDER: PRJNA674371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12974363_1.fastq.gz	Fastqsanger.gz
	SRR12974363_2.fastq.gz	Fastqsanger.gz
	SRR12974364_1.fastq.gz	Fastqsanger.gz
	SRR12974364_2.fastq.gz	Fastqsanger.gz
	SRR12974365_1.fastq.gz	Fastqsanger.gz

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Single-cell sequencing of cortical cells following murine traumatic brain injury [scRNA-seq]

Project description:Traumatic brain injury (TBI) can lead to significant neuropsychiatric problemsand neurodegenerative pathologies, which develop and persist years after injury. Neuroinflammatory processes evolve over this same period. Cortical mRNA analysis showed a robust contribution of microglia to neuroinflammatory pathways that persisted over time post-injury. These data also indicate that inflammation persists in the subacute and chronic time points after TBI, which may affect surrounding neurons, oligodendrocytes and astrocytes. To investigate this hypothesis, a single-cell sequencing approach was used to determine cell-type specific gene expression within the cortex 7 dpi with and without microglial depletion.

2020-11-15 | GSE160763 | GEO

Cortical neuropathology RNA expression time-course after diffuse traumatic brain injury

Project description:Traumatic brain injury (TBI) can lead to significant neuropsychiatric problems and neurodegenerative pathologies, which develop and persist years after injury. Neuroinflammatory processes evolve over this same period. Therefore, we aimed to determine the contribution of microglia to neuropathology at acute (1-day post-injury; dpi), subacute (7 dpi), and chronic (30 dpi) time-points. Microglia were depleted with PLX5622, a CSF1R antagonist, prior to midline fluid percussion injury in male mice and cortical neuropathology/inflammation was assessed using a neuropathology mRNA panel. NanoString Neuropathology gene expression panel was used to quantify expression from RNA microdissected from the mouse cortex.

2020-11-15 | GSE160651 | GEO

Cortical neuropathology RNA expression time-course after diffuse traumatic brain injury

Project description:Cortical neuropathology RNA expression time-course after diffuse traumatic brain injury

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Astrocyte-specific deletion of SOX2 promotes recovery after traumatic brain injury

Project description:Injury to the adult brain induces activation of resident astrocytes, which serves as a compensatory response modulating tissue damage and recovery. However, the mechanism governing astrocyte activation and the role of reactive astrocytes remain largely unknown. Here we show that SOX2, a transcription factor critical for stem cells and brain development, is also required for injury-induced activation of adult cortical astrocytes. Genome-wide ChIP-seq analysis reveals that SOX2 binds to regulatory regions of genes associated with signaling pathways controlling reactive gliosis, such as Socs3, Nr2e1, Notch1, and Akt2. Inducible deletion of Sox2 in adult astrocytes greatly diminishes their response to traumatic injury and, most unexpectedly, restricts injury-induced cortical loss. Together, these results uncover an essential role of SOX2 in terminally differentiated cells and implicate that SOX2-dependent reactive astrocytes may be targeted for regeneration after traumatic brain injury.

2018-02-22 | GSE85213 | GEO

An integrated analysis of gut microbiota and the brain transcriptome reveals host-gut microbiota interactions following traumatic brain injury

Project description:Objectives: The aim of this study was to reveal the transcriptomic profile of the cerebral cortex in traumatic brain injury (TBI) mice. Methods: A controlled cortical impact (CCI) device was used to establish a TBI model. The gene expression in the cerebral cortex was detected by whole-transcriptome sequencing (RNA-Seq).

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Gene expression profiles after traumatic brain injury

Project description:Time dependent-profiles in the gene expression level following lateral moderate fluid percussion injury in the rat brain We used microarray to elucidate relationship between the alteration of gene expression levels and the progression of brain damages following traumatic brain injury. To examine the levels of gene expression in the early phase of traumatic brain injury, we analyzed the gene expression at 3, 6, 12, and 48 h after trauma using the lateral moderate fluid percussion TBI model. The ratios of the gene expression level were compared between chips corresponding to the 3, 6 and 12 h fluid percussion groups and the sham group chips. On the other hand, the rations of gene expression level after 48 h FPI were compared with 48 h sham chip, because the gene expression levels of 48 h sham chip were distinct from sham group chips (3, 6 and 12 h) in the cluster and principal components analyses.

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LFQ proteomics of mouse GABAergic interneurons during traumatic brain injury

Project description:Unilateral Traumatic Brain Injury (TBI) causes functional disturbances of the neuronal networks spreading even to the undamaged cortical hemisphere. The phenomenon, referred to as transhemispheric diaschisis, is suggested to be mediated by an imbalance of the strength of glutamatergic, excitatory vs. GABAergic, inhibitory neurotransmission. Here we present evidence that a switch in expression of α Subunits of pore-forming L-Type voltage-gated calcium channels (VGCC), by an expression of CaV1.3 and simultaneous ablation of CaV1.2 in GABAergic interneurons could balance early cortical disturbances manifested as contralateral hyperexcitability in the early phase after TBI. The switch of the VGCC alpha Subunits in GABAergic interneurons was detected using the GAD67-GFP (Glutamate Decarboxylase 67 – Green Fluorescent Protein) Knock-in mouse line. Mice received a TBI with a Controlled Cortical Impact (CCI) to the primary motor and somatosensory cortex at postnatal day 19-21 under anesthesia in vivo. Single GFP+ interneurons located in the undamaged, contralateral cortex were isolated by Fluorescence-Activated Cell Sorting (FACS) and further analyzed by Mass Spectrometry (MS). The switch was associated with an increased excitability of Somatostatin (SST) interneurons and extracellular network activity in acute brain slices in Microelectrode Array (MEA) recordings, which could be restored in presence of isradipine (100 nM), which selectively blocks CaV1.3-containing VGCCs. These data suggest that a switch in alpha.subunits of VGCCs expressed on SST-positive interneurons stabilizes early hyperactivity of the contralateral cortical network at 72 h after TBI, thereby promoting an adaptive mechanism to counterbalance post-traumatic hyperexcitabilty that might lead to epileptogenesis.

2022-01-03 | PXD023551 | Pride

The meningeal transciptional response to traumatic brain injury and aging [scRNA-seq]

Project description:The meningeal transciptional response to traumatic brain injury and aging [scRNA-seq]

| PRJNA852800 | ENA

Exercise intensity and sex alter neurometabolic, transcriptional, and functional recovery following traumatic brain injury.

Project description:In order to assess the impact of treadmill exercise on traumatic brain injury outcomes, we subjected male and female swiss webster mice to a controlled cortical impact (CCI), followed by 10 days of sedentary, low-, moderate-, or high-intensity treadmill exercise. Outcome measures included neurometabolic function, cognitive recovery, oxidative stress, pathophysiology, and single nuclei RNA sequencing (snRNA seq). The snRNA seq study was conducted on both male and female mice, and included a total of 2 replicates (each was a pool of 2 tissue samples) from each of the following groups: male sham sedentary, male CCI sedentary, male CCI low, male CCI high, female sham sedentary, female CCI sedentary, female CCI low, female CCI high. Our data reveal exercise intensity- and sex-dependent effects of treadmill exercise following injury. Transcriptomic changes were largely limited to the low-intensity exercised CCI males.

2023-08-01 | GSE226072 | GEO

Effect of traumatic brain injury on gene expression in bone.

Project description:It is clinically known, that patients often develop osteoporosis following traumatic brain injury (TBI). To enable a better understanding of the underlying mechanism, we developed a murine TBI model. Mice received a controlled cortical impact inducing a TBI. Expression analysis of the femur 3 days following the injury should reveal the regulated genes. We observed a strong downregulation of osteoblast genes, suggesting an inhibition of bone formation. Furthermore, the beta2-adrenoreceptor was downregulated, what is supposed to be induced by the increased adrenergic signaling in these mice.

2024-01-17 | GSE253133 | GEO

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