ArticleTranslational psychiatry2016
Toward dissecting the etiology of schizophrenia: HDAC1 and DAXX regulate GAD67 expression in an in vitro hippocampal GABA neuron model.
Article in Translational psychiatry, 2016. 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, 27 citations in OpenAlex.
- Clusterin Regulates the Mechanisms of Neuroinflammation and Neuronal Circuit Impairment in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- HIRA vs. DAXX: the two axes shaping the histone H3.3 landscape.Experimental & molecular medicine · 2024Review
- Disturbed circadian rhythm and retinal degeneration in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2023Article
- Chronic jet lag-like conditions dysregulate molecular profiles of neurological disorders in nucleus accumbens and prefrontal cortex.Frontiers in neuroinformatics · 2022Article
- The emerging role of chromatin remodelers in neurodevelopmental disorders: a developmental perspective.Cellular and molecular life sciences : CMLS · 2021Review
- NADScience advances · 2020Article
- Dysregulation of Epigenetic Control Contributes to Schizophrenia-Like Behavior in Ebp1International journal of molecular sciences · 2020Article
- Podocyte histone deacetylase activity regulates murine and human glomerular diseases.The Journal of clinical investigation · 2019Article
- Association of Mental Health-Related Proteins DAXX, DRD3, and DISC1 With the Progression and Prognosis of Chondrosarcoma.Frontiers in molecular biosciences · 2019Article
- GAD1 alternative transcripts and DNA methylation in human prefrontal cortex and hippocampus in brain development, schizophrenia.Molecular psychiatry · 2018Article
- Programming for increased expression of hippocampal GAD67 mediated the hypersensitivity of the hypothalamic-pituitary-adrenal axis in male offspring rats with prenatal ethanol exposure.Cell death & disease · 2018Article
- Epigenetic Regulation of Glutamic Acid Decarboxylase 67 in a Hippocampal Circuit.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- HDAC1 links early life stress to schizophrenia-like phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders.Frontiers in behavioral neuroscience · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Schizophrenia (SZ) is associated with GABA neuron dysfunction in the hippocampus, particularly the stratum oriens of sector CA3/2. A gene expression profile analysis of human postmortem hippocampal tissue followed by a network association analysis had shown a number of genes differentially regulated in SZ, including the epigenetic factors HDAC1 and DAXX. To characterize the contribution of these factors to the developmental perturbation hypothesized to underlie SZ, lentiviral vectors carrying short hairpin RNA interference (shRNAi) for HDAC1 and DAXX were used. In the hippocampal GABA neuron culture model, HiB5, transduction with HDAC1 shRNAi showed a 40% inhibition of HDAC1 mRNA and a 60% inhibition of HDAC1 protein. GAD67, a enzyme associated with GABA synthesis, was increased twofold (mRNA); the protein showed a 35% increase. The expression of DAXX, a co-repressor of HDAC1, was not influenced by HDAC1 inhibition. Transduction of HiB5 cells with DAXX shRNAi resulted in a 30% inhibition of DAXX mRNA that translated into a 90% inhibition of DAXX protein. GAD1 mRNA was upregulated fourfold, while its protein increased by ~30%. HDAC1 expression was not altered by inhibition of DAXX. However, a physical interaction between HDAC1 and DAXX was demonstrated by co-immunoprecipitation. Inhibition of HDAC1 or DAXX increased expression of egr-1, transcription factor that had previously been shown to regulate the GAD67 promoter. Our in vitro results point to a key role of both HDAC1 and DAXX in the regulation of GAD67 in GABAergic HiB5 cells, strongly suggesting that these epigenetic/transcription factors contribute to mechanisms underlying GABA cell dysfunction in SZ.
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