ArticleJournal of molecular neuroscience : MN2020
Transient Forebrain Ischemia Induces Differential Bdnf Transcript Expression and Histone Acetylation Patterns in the Rat Hippocampus.
Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- ErbB signaling in brain injury regeneration: Pathway interactions and therapeutic potential.Neural regeneration research · 2026Article
- Single-Nucleus RNA Sequencing of HDAC6 Inhibition in Resolving Doxorubicin-Induced Cognitive Impairment.Molecular neurobiology · 2025Article
- Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook.Frontiers in genetics · 2025Review
- Brain-Derived Neurotrophic Factor in Pediatric Acquired Brain Injury and Recovery.Biomolecules · 2024Review
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- HDACi protects against vascular cognitive impairment from CCH injury via induction of BDNF-related AMPA receptor activation.Journal of cellular and molecular medicine · 2021Article
- HDAC6 in Diseases of Cognition and of Neurons.Cells · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Forebrain ischemia induces delayed, selective neuronal death in hippocampal CA1. It has been established that BDNF (brain-derived neurotrophic factor) is an important factor in ischemic injury. However, the exact mechanism of BDNF expression in the hippocampus after ischemia is unclear. We found that the decrease of BDNF protein expression in hippocampal CA1 was associated with a decrease of Bdnf transcript IV expression in the same region of the rats after ischemia/reperfusion (I/R). In hippocampal CA3 and DG, the results showed increased expression of BDNF protein and transcripts I, IIc, III, IV, VI, and X1. Furthermore, at the Bdnf promoters, I/R led to decreased H3K27ac, increased H3K9ac, and H3K14ac in CA1; increased H3K9ac, H3K14ac, and H3K27ac in CA3; no significant change of H3K9ac, H3K14ac, and H3K27ac in DG. HDAC inhibitor SAHA increased the expression of Bdnf transcripts IV, VI, and X1 in CA1. These findings suggest a potential of modulation Bdnf transcript expression to resolve ischemic brain injury through histone acetylation patterns at the Bdnf promoters.
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Registered trials
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