ArticleCell & bioscience2021
Mettl14-mediated m6A modification modulates neuron apoptosis during the repair of spinal cord injury by regulating the transformation from pri-mir-375 to miR-375.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting intracellular mRNA mJournal of advanced research · 2026Review
- Spinal motor neuron degeneration after brachial plexus avulsion: mechanisms and therapeutic targets.Frontiers in neuroscience · 2026Review
- METTL3-Driven m6A Epigenetic Remodeling of lncRNA-AU020206 Stabilizes SLC7A11 via YTHDC2 Attenuates Apoptosis and Ferroptosis in Cerebral Ischemia/Reperfusion Injury.Biomolecules · 2025Article
- The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025Review
- Characterization of the Expressions and m6A Methylation Modification Patterns of mRNAs and lncRNAs in a Spinal Cord Injury Rat Model.Molecular neurobiology · 2025Article
- Mechanism of Mettl14 regulating AIM2 inflammasome activation and neuronal apoptosis and pyroptosis in spinal cord injury by mediating PPARγ m6A methylation.Journal of physiology and biochemistry · 2024Article
- N6-Methyladenosine Methylation of mRNA in Cell Apoptosis.Molecular neurobiology · 2024Review
- Mechanism of Fat Mass and Obesity-Related Gene-Mediated Heme Oxygenase-1 m6A Modification in the Recovery of Neurological Function in Mice with Spinal Cord Injury.Orthopaedic surgery · 2024Article
- RNA modification: mechanisms and therapeutic targets.Molecular biomedicine · 2023Review
- METTL3 Affects Spinal Cord Neuronal Apoptosis by Regulating Bcl-2 m6A Modifications After Spinal Cord Injury.Neurospine · 2023Article
- Silencing METTL3 Stabilizes Atherosclerotic Plaques by Regulating the Phenotypic Transformation of Vascular Smooth Muscle Cells via the miR-375-3p/PDK1 Axis.Cardiovascular drugs and therapy · 2023Article
- Upregulation of UBR1 m6A Methylation by METTL14 Inhibits Autophagy in Spinal Cord Injury.eNeuro · 2023Article
- USP1/UAF1-Stabilized METTL3 Promotes Reactive Astrogliosis and Improves Functional Recovery after Spinal Cord Injury through mThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Construction of an acute myeloid leukemia prognostic model based on m6A-related efferocytosis-related genes.Frontiers in immunology · 2023Article
- The role, mechanism, and application of RNA methyltransferase METTL14 in gastrointestinal cancer.Molecular cancer · 2022Review
- METTL14 promotes apoptosis of spinal cord neurons by inducing EEF1A2 m6A methylation in spinal cord injury.Cell death discovery · 2022Article
- N6-methyladenosine modification: A potential regulatory mechanism in spinal cord injury.Frontiers in cellular neuroscience · 2022Review
- Mechanism of Ferroptosis and Its Role in Spinal Cord Injury.Frontiers in neurology · 2022Review
- Correction to: Mettl14-mediated m6A modification modulates neuron apoptosis during the repair of spinal cord injury by regulating the transformation from pri-mir-375 to miR-375.Cell & bioscience · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSpinal cord injury (SCI) is a disabling disorder, resulting in neurological impairments. This study investigated the mechanism of methyltransferase-like 14 (Mettl14) on apoptosis of spinal cord neurons during SCI repair by mediating pri-microRNA (miR) dependent N6-methyladenosine (m6A) methylation.
methodsThe m6A content in total RNA and Mettl14 levels in spinal cord tissues of SCI rats were detected. Mettl14 expression was intervened in SCI rats to examine motor function, neuron apoptosis, and recovery of neurites. The cell model of SCI was established and intervened with Mettl14. miR-375, related to SCI and positively related to Mettl14, was screened out. The expression of miR-375 and pri-miR-375 after Mettl14 intervention was detected. The expression of pri-miR-375 combined with DiGeorge critical region 8 (DGCR8) and that modified by m6A was detected. Furthermore, the possible downstream gene and pathway of miR-375 were analysed. SCI cell model with Mettl14 intervention was combined with Ras-related dexamethasone-induced 1 (RASD1)/miR-375 intervention to observe the apoptosis.
resultsMettl14 level and m6A content in spinal cord tissue were significantly increased. After Mettl14 knockdown, the injured motor function was restored and neuron apoptosis was reduced. In vitro, Mettl14 silencing reduced the apoptosis of SCI cells; miR-375 was reduced and pri-miR-375 was increased; miR-375 targeted RASD1. Silencing Mettl14 inactivated the mTOR pathway. The apoptosis in cells treated with silencing Mettl14 + RASD1/miR-375 was inhibited.
conclusionsMettl14-mediated m6A modification inhibited RASD1 and induced the apoptosis of spinal cord neurons in SCI by promoting the transformation of pri-miR-375 to mature miR-375.
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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 OpenQuestion graph.