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Glial immune-related pathways as mediators of closed head TBI effects on behavior and lethality in Drosophila

ABSTRACT: Glial immune-related pathways as mediators of closed head TBI effects on behavior and lethality in Drosophila

PROVIDER: PRJNA690250 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13376483.fastq.gz	Fastqsanger.gz
	SRR13376484.fastq.gz	Fastqsanger.gz
	SRR13376485.fastq.gz	Fastqsanger.gz
	SRR13376486.fastq.gz	Fastqsanger.gz
	SRR13376487.fastq.gz	Fastqsanger.gz

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Project description:Astrocytes, the most abundant glial cells in the central nervous system (CNS), play a critical role in brain injury responses. While NeuroD1 overexpression in astrocytes has been shown to reverse glial scar formation and promote tissue repair in mouse models of traumatic brain injury (TBI), the underlying molecular mechanisms remain incompletely understood. To address this, we performed single-cell transcriptomic analysis on a controlled cortical impact (CCI) mouse model using recombinant adeno-associated virus (rAAV)-mediated astrocyte-specific NeuroD1 overexpression.Our findings demonstrate that NeuroD1 overexpression suppresses microglial activation and mitigates brain damage post-TBI. Single-cell RNA sequencing revealed significant shifts in astrocyte subtypes, with upregulated neuroinflammatory pathways and downregulated oxygen metabolism in TBI mice. Conversely, NeuroD1 overexpression reshaped astrocyte subpopulation dynamics, enhanced oxygen metabolism-related gene expression, and attenuated neuroinflammatory signaling. This study provides a comprehensive transcriptomic dataset detailing cellular and astrocyte subtype-specific changes following NeuroD1-mediated brain repair. These insights advance our understanding of cell fate modulation in TBI and support the development of NeuroD1-based gene therapies, offering a valuable resource for future TBI research and therapeutic strategies.

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MS sequencing of GFAP fragments from TBI patients CSF

Project description:Protein Glial fibrillary acidic protein, GFAP fragment identification (breakdown products, BDPs) and their label free peptide/ion quantification of GFAP immunoprecipitated from TBI patient's cerebrospinal fluid using a polyclonal anti-GFAP antibody. GFAP fragments of distinct molecular weights were cut out and in gel-digested prior to LC-MS/MS using Proteome discoverer 1.4. Peptide results from PD output files were combined from four TBI patients, 6 CSF samples to generate a multiconsensus peptide coverage map for each molecular weight fragment. See Wanner et al., BioRXiv 2025: https://doi.org/10.1101/2025.08.01.668181.

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Hippocampus-Cerebellum Axis Specific Transcriptomic Stratification to Discriminate Mild from Moderate TBI

Project description:The variations of psycho- and physiological deficits caused by TBI correlate with the degree of brain injury. However, the objective stratification of TBI is yet elusive. A modified closed-head injury Marmarou model was used based on the release of a 500 gram steel slug on top of the rat skull from a height of 100 cm or 120 cm to induce differential injury models for mild TBI and moderate TBI, respectively. The skull was covered by a helmet to mimic the warfighter’s condition in theater. The hippocampus was at the focal point of injury, and the cerebellum, was susceptible to diffused shock (secondary injury). The HC-CB axis coordinates visuomotor performance, which is known to be vulnerable to TBI. The rats that received moderate TBI showed deficient visuomotor performance by the Barnes maze test for longer time periods than those inflicted with mild TBI. The time resolved and HC-CB specific transcriptomic analysis focused on genes that enabled discrimination of mild from moderate TBI at 14d post injury which is equivalent to nearly 1.5 years of human lifetime. The functional analysis elucidated an active healing mechanism in the HC exposed to mild TBI. In contrast, moderate TBI caused delayed healing and active cell death in the HC. In conclusion, the graded brain injuries differentially implicated the HC-CB axis, despite the use of a helmet to reduce the impact. Time resolved functional dynamics informed the distinct consequences of mild vs. moderate TBI.

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