ArticleHuman genomics2023
The RNA m6A modification might participate in microglial activation during hypoxic-ischemic brain damage in neonatal mice.
Article in Human genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Dexmedetomidine inhibits microglia activation, neuroinflammation, and glycolysis in postoperative cognitive dysfunction by promoting YTHDF2-mediated PKM2 mRNA degradation.Molecular and cellular biochemistry · 2026Article
- m6A RNA methylation in neural plasticity, brain aging, and neurodegenerative vulnerability.Molecular brain · 2026Review
- Regulation of FTO on PDCD5 mRNA stability to mediate neuron apoptosis in rats with hypoxic-ischemic brain damage.Translational neuroscience · 2026Article
- Mechanisms of Fat Mass and Obesity-Associated Protein in Regulating Cognitive Impairment Induced by Sevoflurane Anesthesia in Neonatal Rats.Neurochemical research · 2025Article
- Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025Review
- Extracellular vesicle signatures from eye lavage as novel non-invasive biomarkers for hypoxic ischaemic insult-findings from a neonatal mouse model.Frontiers in medical technology · 2025Article
- BARD1-mediated stabilization of METTL14 promotes retinal neovascularization by m6A-modifying MXD1 mRNA on a YTHDF2-dependent manner.Theranostics · 2025Article
- Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases.Human genomics · 2024Review
- Article
- The indispensability of methyltransferase-like 3 in the immune system: from maintaining homeostasis to driving function.Frontiers in immunology · 2024Review
- Regulatory Network of Methyltransferase-Like 3 in Stem Cells: Mechanisms and Medical Implications.Cell transplantationReview
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe RNA m6A modification has been implicated in multiple neurological diseases as well as macrophage activation. However, whether it regulates microglial activation during hypoxic-ischemic brain damage (HIBD) in neonates remains unknown. Here, we aim to examine whether the m6A modification is involved in modulating microglial activation during HIBD. We employed an oxygen and glucose deprivation microglial model for in vitro studies and a neonatal mouse model of HIBD. The brain tissue was subjected to RNA-seq to screen for significant changes in the mRNA m6A regulator. Thereafter, we performed validation and bioinformatics analysis of the major m6A regulators.
resultsRNA-seq analysis revealed that, among 141 m6A regulators, 31 exhibited significant differential expression (FC (abs) ≥ 2) in HIBD mice. We then subjected the major m6A regulators Mettl3, Mettl14, Fto, Alkbh5, Ythdf1, and Ythdf2 to further validation, and the results showed that all were significantly downregulated in vitro and in vivo. GO analysis reveals that regulators are mainly involved in the regulation of cellular and metabolic processes. The KEGG results indicate the involvement of the signal transduction pathway.
conclusionsOur findings demonstrate that m6A modification of mRNA plays a crucial role in the regulation of microglial activation in HIBD, with m6A-associated regulators acting as key modulators of microglial activation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.