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Inhibition of METTL3 protect against traumatic brain injury

ABSTRACT: Inhibition of METTL3 protect against traumatic brain injury

PROVIDER: PRJNA1102868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28758461_1.fastq.gz	Fastqsanger.gz
	SRR28758461_2.fastq.gz	Fastqsanger.gz
	SRR28758462_1.fastq.gz	Fastqsanger.gz
	SRR28758462_2.fastq.gz	Fastqsanger.gz
	SRR28758463_1.fastq.gz	Fastqsanger.gz

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Inhibition of METTL3 protect against traumatic brain injury

Project description:Researchers recently identified STM2457 as a first-in-class catalytic inhibitor of METTL3 and observed a promising therapeutic effect on acute myeloid leukemia. However, it is crucial to note that the existence of the blood-brain barrier (BBB) limit the efficiency of drugs entering the brain to a large extent. In order to effectively deliver METTL3 inhibitor STM2457 to the brain, we generated RVG29 (a BBB-penetrating peptide)-based modified nanoparticle system loaded with STM2457 (abbreviated as RVG-nSTM system) that targets the brain. Specifically, a mixture of STM2457, PLGA20K-mPEG2K, and PLGA20K-PEG5K-MAL was used to prepare nSTM, which was further modified with RVG29 peptide. We investigated the impact of RVG-nSTM on neuroinflammation post-TBI in mice. We performed a total RNA-seq analysis, and observed distinct gene distributions on the volcano plot. A Venn diagram revealed that 3385 genes were differentially expressed in the TBI group compared to the sham group, and treatment with RVG-nSTM reversed the expression of 1941 of these genes . The subsequent GO and KEGG analyses showed that these 1941 genes were primarily enriched in the context of inflammatory response and inflammation-related pathways. These findings were further corroborated by the observation that RVG-nSTM treatment leads to a substantial reversal of the hyperactive microglial states that are induced by TBI . Above all, RVG-nSTM could be a promising agent for the treatment of neuroinflammation after acute brain injury.

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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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