ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2021
TET3 regulates DNA hydroxymethylation of neuroprotective genes following focal ischemia.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- Epigenetic mechanisms in traumatic brain injury: a focus on astrocytes and therapeutic implications.Journal of neuroinflammation · 2026Review
- Spatial transcriptomics reveals brain-wide circadian disruption in an Alzheimer's disease model.bioRxiv : the preprint server for biology · 2026Article
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- MicroRNA profiling in post-mortem spinal cord of C9ORF72-related ALS patients reveals molecular pathways involved in motor neuron degeneration.Frontiers in neuroscience · 2026Article
- TET3-Interacting LncRNA TILR Is Essential for DNA Hydroxymethylation-Mediated Neuroprotection After Ischemic Stroke.Stroke · 2025Article
- DNA methylation and hydroxymethylation dynamics in the aging brain and its impact on ischemic stroke.Neurochemistry international · 2025Review
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction.IBRO neuroscience reports · 2025Article
- Therapeutic Potential of Intravenous miR-21 Mimic after Stroke Following STAIR Criteria.Translational stroke research · 2025Article
- Potential therapeutic targets for ischemic stroke in pre-clinical studies: Epigenetic-modifying enzymes DNMT/TET and HAT/HDAC.Frontiers in pharmacology · 2025Review
- Cognitive Impairment Mechanisms in High-Altitude Exposure: Proteomic and Metabolomic Insights.Journal of proteome research · 2024Article
- Role of transcription factors, noncoding RNAs, epitranscriptomics, and epigenetics in post-ischemic neuroinflammation.Journal of neurochemistry · 2024Review
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- Stroke triggers dynamic mNeurochemistry international · 2024Article
- Selective Estrogen Receptor Modulators' (SERMs) Influence onInternational journal of molecular sciences · 2024Article
- Recent Advances and Therapeutic Implications of 2-Oxoglutarate-Dependent Dioxygenases in Ischemic Stroke.Molecular neurobiology · 2024Review
- TET2-mediated ECM1 hypomethylation promotes the neovascularization in active proliferative diabetic retinopathy.Clinical epigenetics · 2024Article
- An Overview of Global, Local, and Base-Resolution Methods for the Detection of 5-Hydroxymethylcytosine in Genomic DNA.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Article
- Post-stroke depression: epigenetic and epitranscriptomic modifications and their interplay with gut microbiota.Molecular psychiatry · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The 5-hydroxymethylcytosine (5hmC) epigenetic modification is highly enriched in the CNS and a critical modulator of neuronal function and development. We found that cortical 5hmC was enhanced from 5 min to three days of reperfusion following focal ischemia in adult mice. Blockade of the 5hmC-producing enzyme ten-eleven translocase 3 (TET3) increased edema, infarct volume, and motor function impairments. To determine the mechanism by which TET3 provides ischemic neuroprotection, we assessed the genomic regions where TET3 modulates 5hmC. Genome-wide sequencing analysis of differentially hydroxymethylated regions (DhMRs) revealed that focal ischemia robustly increased 5hmC at the promoters of thousands of genes in a TET3-dependent manner. TET3 inhibition reduced 5hmC at the promoters of neuroprotective genes involved in cell survival, angiogenesis, neurogenesis, antioxidant defense, DNA repair, and metabolism demonstrating a role for TET3 in endogenous protection against stroke. The mRNA expression of several genes with known involvement in ischemic neuroprotection were also reduced with TET3 knockdown in both male and female mice, establishing a correlation between decreased promoter 5hmC levels and decreased gene expression. Collectively, our results indicate that TET3 globally increases 5hmC at regulatory regions and overwhelmingly modulates 5hmC in several neuroprotective pathways that may improve outcome after ischemic injury.
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