ArticleJournal of cellular and molecular medicine2020
HDAC inhibitor protects chronic cerebral hypoperfusion and oxygen-glucose deprivation injuries via H3K14 and H4K5 acetylation-mediated BDNF expression.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 22 citations in OpenAlex.
- Molecular modeling to simulation: insights into Gaussian QSAR, molecular docking, and DFT for identification of HDAC3 inhibitors for neurocognitive vascular dementia.Scientific reports · 2025Article
- Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- H3K14: A histone site closely related to diseases.Journal of Cancer · 2025Review
- Tangeretin confers neuroprotection, cognitive and memory enhancement in global cerebral ischemia in rats.3 Biotech · 2024Article
- Nasal Administration of bFGF-Loaded Nanoliposomes Attenuates Neuronal Injury and Cognitive Deficits in Mice with Vascular Dementia Induced by Repeated Cerebral Ischemia‒Reperfusion.International journal of nanomedicine · 2024Article
- Assessment of Four Serum Biochemical Markers in Elderly Patients with Vascular Dementia after Cerebral Infarction and Their Response to Donepezil and Idebenone.Journal of neurological surgery. Part B, Skull base · 2023Article
- Neuronal Responses to Ischemia: Scoping Review of Insights from Human-Derived In Vitro Models.Cellular and molecular neurobiology · 2023Article
- Role of SH3GLB1 in the regulation of CD133 expression in GBM cells.BMC cancer · 2023Article
- Endothelial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Triptolide protects against white matter injury induced by chronic cerebral hypoperfusion in mice.Acta pharmacologica Sinica · 2022Article
- HDACi protects against vascular cognitive impairment from CCH injury via induction of BDNF-related AMPA receptor activation.Journal of cellular and molecular medicine · 2021Article
- Tubulin and Tubulin Posttranslational Modifications in Alzheimer's Disease and Vascular Dementia.Frontiers in aging neuroscience · 2021Review
- HDAC inhibitor protects chronic cerebral hypoperfusion and oxygen-glucose deprivation injuries via H3K14 and H4K5 acetylation-mediated BDNF expression.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular dementia (VaD) is the second most common cause of dementia, but the treatment is still lacking. Although many studies have reported that histone deacetylase inhibitors (HDACis) confer protective effects against ischemic and hypoxic injuries, their role in VaD is still uncertain. Previous studies shown, one HDACi protected against cognitive decline in animals with chronic cerebral hypoperfusion (CCH). However, the underlying mechanisms remain elusive. In this study, we tested several 10,11-dihydro-5H-dibenzo[b,f]azepine hydroxamates, which act as HDACis in the CCH model (in vivo), and SH-SY5Y (neuroblastoma cells) with oxygen-glucose deprivation (OGD, in vitro). We identified a compound 13, which exhibited the best cell viability under OGD. The compound 13 could increase, in part, the protein levels of brain-derived neurotrophic factor (BDNF). It increased acetylation status on lysine 14 residue of histone 3 (H3K14) and lysine 5 of histone 4 (H4K5). We further clarified which promoters (I, II, III, IV or IX) could be affected by histone acetylation altered by compound 13. The results of chromatin immunoprecipitation and Q-PCR analysis indicate that an increase in H3K14 acetylation leads to an increase in the expression of BDNF promoter II, while an increase in H4K5 acetylation results in an increase in the activity of BDNF promoter II and III. Afterwards, these cause an increase in the expression of BDNF exon II, III and coding exon IX. In summary, the HDACi compound 13 may increase BDNF specific isoforms expression to rescue the ischemic and hypoxic injuries through changes of acetylation on histones.
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