ArticleCellular and molecular neurobiology2022
Role of Altered Expression, Activity and Sub-cellular Distribution of Various Histone Deacetylases (HDACs) in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis.
Article in Cellular and molecular neurobiology, 2022. 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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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Genome-wide rare copy number variations potentially associated with drug resistance in epilepsy.Scientific reports · 2026Article
- Pyk2 dysregulation in temporal lobe epilepsy: insights from human resected tissues and pharmacological modulation in a rodent model.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Chidamide Is Screened to Suppress Epileptogenesis in Mice Models via Blocking Histone Deacetylase 1.CNS neuroscience & therapeutics · 2026Article
- Histone and non-histone (de)acetylation impact on the blood-brain barrier.Fluids and barriers of the CNS · 2026Review
- Altered Fibronectin-α5β1 Integrin-Src Signalling Pathway Drives Network Hyperexcitability in the Hippocampal Formation and Anterior Temporal Lobe in Temporal Lobe Epilepsy.Neurochemical research · 2026Article
- Exploring histone acetylation in ischemic stroke: CREBBP and CKAP4 as candidate biomarkers linked to histone acetylation networks.Frontiers in pharmacology · 2026Article
- HDAC1 Promotes Hippocampal Neuronal Pyroptosis in Epileptic Mice Through the miR-15a-5p/Caspase-1 Axis.Neurochemical research · 2025Article
- Epigenetic Mechanisms in the Pathophysiology and Progression of Epilepsy: A Comprehensive Review of Experimental and Clinical Studies.Current neuropharmacology · 2025Review
- Unveiling the role of histone deacetylases in neurological diseases: focus on epilepsy.Biomarker research · 2024Review
- The Role of Histone Deacetylases in NLRP3 Inflammasomesmediated Epilepsy.Current molecular medicine · 2024Review
- Treatment of Status Epilepticus after Traumatic Brain Injury Using an Antiseizure Drug Combined with a Tissue Recovery Enhancer Revealed by Systems Biology.International journal of molecular sciences · 2023Article
- HAT- and HDAC-Targeted Protein Acetylation in the Occurrence and Treatment of Epilepsy.Biomedicines · 2022Review
- Multi-omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy.Epilepsia open · 2022Review
- Histone deacetylase 10, a potential epigenetic target for therapy.Bioscience reports · 2021Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Histone deacetylases (HDACs) have been described to have both neurotoxic and neuroprotective roles, and partly, depend on its sub-cellular distribution. HDAC inhibitors have a long history of use in the treatment of various neurological disorders including epilepsy. Key role of HDACs in GABAergic neurotransmission, synaptogenesis, synaptic plasticity and memory formation was demonstrated whereas very less is known about their role in drug-resistant epilepsy pathologies. The present study was aimed to investigate the changes in the expression of HDACs, activity and its sub-cellular distribution in mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) patients. For this study, surgically resected hippocampal tissue specimens of 28 MTLE-HS patients and 20 hippocampus from post-mortem cases were obtained. Real-time PCR was done to analyse the mRNA expression. HDAC activity and the protein levels of HDACs in cytoplasm as well as nucleus were measured spectrophotometrically. Further, sub-cellular localization of HDACs was characterized by immunofluorescence. Significant upregulation of HDAC1, HDAC2, HDAC4, HDAC5, HDAC6, HDAC10 and HDAC11 mRNA were observed in MTLE-HS. Alterations in the mRNA expression of glutamate and gamma-aminobutyric acid (GABA) receptor subunits have been also demonstrated. We observed significant increase of HDAC activity and nuclear level of HDAC1, HDAC2, HDAC5 and HDAC11 in the hippocampal samples obtained from patients with MTLE-HS. Moreover, we found altered cytoplasmic level of HDAC4, HDAC6 and HDAC10 in the hippocampal sample obtained from patients with MTLE-HS. Alterations in the level of HDACs could potentially be part of a dynamic transcription regulation associated with MTLE-HS. Changes in cytoplasmic level of HDAC4, 6 and 10 suggest that cytoplasmic substrates may play a crucial role in the pathophysiology of MTLE-HS. Knowledge regarding expression pattern and sub-cellular distribution of HDACs may help to devise specific HDACi therapy for epilepsy.
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