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Screen of traumatic brain injury-associated genes from lncRNA m6A-modified transcriptomes in the cerebral cortex of mice after repetitive mild traumatic brain injury

ABSTRACT: Screen of traumatic brain injury-associated genes from lncRNA m6A-modified transcriptomes in the cerebral cortex of mice after repetitive mild traumatic brain injury

PROVIDER: PRJNA1212210 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32039327_1.fastq.gz	Fastqsanger.gz
	SRR32039327_2.fastq.gz	Fastqsanger.gz
	SRR32039328_1.fastq.gz	Fastqsanger.gz
	SRR32039328_2.fastq.gz	Fastqsanger.gz
	SRR32039329_1.fastq.gz	Fastqsanger.gz

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Screen of traumatic brain injury-associated genes from lncRNA m6A-modified transcriptomes in the cerebral cortex of mice after repetitive mild traumatic brain injury

Project description:N6-methyladenosine (m6A), a prevalent post-transcriptional modification in eukaryotic RNA, plays a significant role in regulating sensory experiences, learning, and injury in the mammalian central nervous system. However, the pattern of lncRNA m6A methylation in the mouse cortex following repetitive mild traumatic brain injury (rmTBI) has not been explored. This study conducted a genome-wide analysis of lncRNA m6A methylation in the mouse cortex using methylated RNA immunoprecipitation sequencing (MeRIP-Seq). Our analysis revealed 43,103 peaks were significantly upregulated or downregulated. Notably, the expression of m6A peaks indicated altered methylation and expression levels of 423 lncRNAs after rmTBI. In addition, employing METTL3 inhibitor STM2457 demonstrated that functional METTL3 was essential for repairing neural damage caused by rmTBI and influenced spatial learning and memory in rmTBI-model mice. Thus, the m6A methylation pattern of lncRNA in the mouse cortex after rmTBI identifies METTL3 as a potential intervention target for epigenetic modification following such injuries.

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Repetitive mild closed head injury in adolescent mice is associated with impaired proteostasis, neuroinflammation, and tauopathy

Project description:Repetitive mild traumatic brain injury (mTBI) in children and adolescents leads to acute and chronic neurological sequelae and is linked by epidemiological data to later life neurodegenerative disease. However, the biological mechanisms connecting early life mTBI to neurodegeneration remain unknown. Using an adolescent mouse repetitive closed head injury (CHI) model that induces progressive cognitive impairment in the absence of overt histopathology, we examined transcriptional and translational changes in neurons isolated from sham and injured brain in the chronic phase after injury. At 14 months, single nuclei RNA sequencing of cortical brain tissue identified disruption of genes associated with neuronal proteostasis in injured mice. Western blot analysis of neurons isolated by immunopanning showed evidence of inflammasome activation, accumulation of misfolded, hyperphosphorylated Tau, and changes in expression of proteins suggestive of impaired translation. Compared to injured wild type, injured interleukin-1 receptor 1 knockout mice, which are protected from post-injury cognitive deficits, had reduced microgliosis and decreased accumulation of pro-interleukin-1 beta and misfolded tau in cortex and cerebellum at six months. Taken together, our findings provide evidence for neuronal inflammasome activation and impaired proteostasis as key mechanisms linking repetitive mTBI in adolescence to later life neurological dysfunction and neurodegeneration.

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