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Journal articles on the topic 'Histone acetylation in brain cells'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Demyanenko, Svetlana, and Svetlana Sharifulina. "The Role of Post-Translational Acetylation and Deacetylation of Signaling Proteins and Transcription Factors after Cerebral Ischemia: Facts and Hypotheses." International Journal of Molecular Sciences 22, no. 15 (2021): 7947. http://dx.doi.org/10.3390/ijms22157947.

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Histone deacetylase (HDAC) and histone acetyltransferase (HAT) regulate transcription and the most important functions of cells by acetylating/deacetylating histones and non-histone proteins. These proteins are involved in cell survival and death, replication, DNA repair, the cell cycle, and cell responses to stress and aging. HDAC/HAT balance in cells affects gene expression and cell signaling. There are very few studies on the effects of stroke on non-histone protein acetylation/deacetylation in brain cells. HDAC inhibitors have been shown to be effective in protecting the brain from ischemi

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Demyanenko, Svetlana, Valentina Dzreyan, and Svetlana Sharifulina. "Histone Deacetylases and Their Isoform-Specific Inhibitors in Ischemic Stroke." Biomedicines 9, no. 10 (2021): 1445. http://dx.doi.org/10.3390/biomedicines9101445.

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Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed. The ischemic stroke generally reduces the gene expression due to suppression of acetylation of histones H3 and H4. Histone deacetylases inhibitors have been shown to be effective in protecting the brain from ischemic damage. Histone deacetylases inhibitors induce neurogenesis and angiogenesis in damaged brain areas promoting functional recovery after cerebral ischemia. However, the role of different histone deacetylases isoforms in the survival and death of brain cells after stroke is s

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Yang, Chao, Lijun Ge, Xiyong Yu, Philip Lazarovici, and Wenhua Zheng. "Artemisinin Confers Cytoprotection toward Hydrogen Peroxide-Induced Cell Apoptosis in Retinal Pigment Epithelial Cells in Correlation with the Increased Acetylation of Histone H4 at Lysine 8." Molecules 29, no. 8 (2024): 1789. http://dx.doi.org/10.3390/molecules29081789.

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Increased oxidative stress is one of the critical pathologies inducing age-related macular degeneration (AMD), characterized by retinal pigment epithelial (RPE) cell damage and death. The unbalanced acetylation and deacetylation of histones have been implicated in AMD pathogenesis or hydrogen peroxide (H2O2)-induced cell damage. Therefore, strategies aimed at controlling the balance between acetylation and deacetylation may effectively protect RPE cells from oxidative damage. Artemisinin is an antimalarial lactone drug derived from Artemisia annua, with antioxidant activity known to modulate h

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Castro, Kamilah, and Patrizia Casaccia. "Epigenetic modifications in brain and immune cells of multiple sclerosis patients." Multiple Sclerosis Journal 24, no. 1 (2018): 69–74. http://dx.doi.org/10.1177/1352458517737389.

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Multiple sclerosis (MS) is a debilitating neurological disease whose onset and progression are influenced by the interplay of genetic and environmental factors. Epigenetic modifications, which include post-translational modification of the histones and DNA, are considered mediators of gene–environment interactions and a growing body of evidence suggests that they play an important role in MS pathology and could be potential therapeutic targets. Since epigenetic events regulate transcription of different genes in a cell type–specific fashion, we caution on the distinct functional consequences t

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Iaconelli, Jonathan, Lucius Xuan, and Rakesh Karmacharya. "HDAC6 Modulates Signaling Pathways Relevant to Synaptic Biology and Neuronal Differentiation in Human Stem-Cell-Derived Neurons." International Journal of Molecular Sciences 20, no. 7 (2019): 1605. http://dx.doi.org/10.3390/ijms20071605.

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Recent studies show that histone deacetylase 6 (HDAC6) has important roles in the human brain, especially in the context of a number of nervous system disorders. Animal models of neurodevelopmental, neurodegenerative, and neuropsychiatric disorders show that HDAC6 modulates important biological processes relevant to disease biology. Pan-selective histone deacetylase (HDAC) inhibitors had been studied in animal behavioral assays and shown to induce synaptogenesis in rodent neuronal cultures. While most studies of HDACs in the nervous system have focused on class I HDACs located in the nucleus (

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Roesler, Prof Rafael, Ms Natalia Hogetop Freire, Dr Caroline Brunetto de Farias, et al. "EPIGENETIC MODULATION OF STEMNESS AND DIFFERENTIATION BY VALPROIC ACID IN MEDULLOBLASTOMA." Neuro-Oncology 26, Supplement_7 (2024): vii19. http://dx.doi.org/10.1093/neuonc/noae158.077.

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Abstract AIMS Changes in epigenetic processes, including histone acetylation, are proposed as key events affecting tumor cell function and the initiation and progression of pediatric brain cancers. Valproic acid (VPA) is an antiepileptic drug that acts partially by inhibiting histone deacetylases (HDACs) and could be repurposed as an epigenetic anticancer therapy. Here, we report VPA-induced alterations in features related to stemness and differentiation in medulloblastoma (MB) cells. METHOD Human MB cells were treated with different concentrations of VPA and cell viability was measured with a

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Lisiero, Dominique Naomi, Horacio Soto, Shanna Fang, Antoni Ribas, Linda Liau, and Robert Prins. "Histone deacetylase inhibitor, LBH589, synergizes with an immunotherapy treatment in an in vivo murine brain tumor model (41.35)." Journal of Immunology 182, no. 1_Supplement (2009): 41.35. http://dx.doi.org/10.4049/jimmunol.182.supp.41.35.

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Abstract Cancer immunotherapy treatments may show low response rates due to an anti-apoptotic tumor environment. We hypothesized a treatment of immunotherapy and histone deacetylase inhibitor, LBH589, could induce tumor cell expression of pro-apoptotic molecules and sensitize these cells to immune mediated cell death. Treatment with adoptive transfer immunotherapy and LBH589 resulted in synergistically reduced s.c. tumor burden, and prolonged survival in an intracranial tumor model. In vivo studies in non-tumor bearing mice treated with this combination therapy showed a 2-fold increase in the

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Espinos, Estelle, Agathe Le Van Thaï, Christelle Pomiès, and Michel J. Weber. "Cooperation between Phosphorylation and Acetylation Processes in Transcriptional Control." Molecular and Cellular Biology 19, no. 5 (1999): 3474–84. http://dx.doi.org/10.1128/mcb.19.5.3474.

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ABSTRACT We previously reported that the activation of the M promoter of the human choline acetyltransferase (ChAT) gene by butyrate and trapoxin in transfected CHP126 cells is blocked by PD98059, a specific mitogen-activated protein kinase kinase (MEK) inhibitor (E. Espinos and M. J. Weber, Mol. Brain Res. 56:118–124, 1998). We now report that the transcriptional effects of histone deacetylase inhibitors are mediated by an H7-sensitive serine/threonine protein kinase. Activation of the ChAT promoter by butyrate and trapoxin was blocked by 50 μM H7 in both transient- and stable-transfection as

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Bergamasco, Maria I., Waruni Abeysekera, Alexandra L. Garnham, et al. "KAT6B is required for histone 3 lysine 9 acetylation and SOX gene expression in the developing brain." Life Science Alliance 8, no. 2 (2024): e202402969. http://dx.doi.org/10.26508/lsa.202402969.

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Heterozygous mutations in the histone lysine acetyltransferase geneKAT6B(MYST4/MORF/QKF) underlie neurodevelopmental disorders, but the mechanistic roles of KAT6B remain poorly understood. Here, we show that loss of KAT6B in embryonic neural stem and progenitor cells (NSPCs) impaired cell proliferation, neuronal differentiation, and neurite outgrowth. Mechanistically, loss of KAT6B resulted in reduced acetylation at histone H3 lysine 9 and reduced expression of key nervous system development genes in NSPCs and the developing cortex, including the SOX gene family, in particularSox2, which is a

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10

Freire, Natália Hogetop, Alice Laschuk Herlinger, Julia Vanini, et al. "Modulation of Stemness and Differentiation Regulators by Valproic Acid in Medulloblastoma Neurospheres." Cells 14, no. 2 (2025): 72. https://doi.org/10.3390/cells14020072.

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Changes in epigenetic processes such as histone acetylation are proposed as key events influencing cancer cell function and the initiation and progression of pediatric brain tumors. Valproic acid (VPA) is an antiepileptic drug that acts partially by inhibiting histone deacetylases (HDACs) and could be repurposed as an epigenetic anticancer therapy. Here, we show that VPA reduced medulloblastoma (MB) cell viability and led to cell cycle arrest. These effects were accompanied by enhanced H3K9 histone acetylation (H3K9ac) and decreased expression of the MYC oncogene. VPA impaired the expansion of

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Soliman, Mahmoud L., and Thad A. Rosenberger. "Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression." Molecular and Cellular Biochemistry 352, no. 1-2 (2011): 173–80. http://dx.doi.org/10.1007/s11010-011-0751-3.

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Baghel, Meghraj Singh, Brijendra Singh, Nisha Patro, Vinay Kumar Khanna, Ishan Kumar Patro, and Mahendra Kumar Thakur. "Poly (I:C) Exposure in Early Life Alters Methylation of DNA and Acetylation of Histone at Synaptic Plasticity Gene Promoter in Developing Rat Brain Leading to Memory Impairment." Annals of Neurosciences 26, no. 3-4 (2019): 35–41. http://dx.doi.org/10.1177/0972753120919704.

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Background: Exposure to adverse environmental conditions such as toxic chemicals, viral infections, and even stress during pregnancy or early life may disrupt the development of normal brain and its functioning leading to incidence of neurodevelopmental disorders at later stages of life. Recently, we reported that poly (I:C) exposure altered synaptic plasticity protein level and impaired memory through activation of microglia cells. Purpose: As epigenetic modifications are involved in memory formation, we have studied methylation of DNA and acetylation of histone at promoters of synaptic plast

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Paine, Danyelle, Nanyun Tang, Yue Hao, et al. "Abstract 4740: Molecular effects of histone deacetylase inhibitor Quisinostat on diffuse midline glioma of the pons." Cancer Research 83, no. 7_Supplement (2023): 4740. http://dx.doi.org/10.1158/1538-7445.am2023-4740.

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Abstract Diffuse Midline Glioma of the pons (DMG) is a lethal, aggressive heterogeneous brain stem tumor. Median overall survival is less than a year, with radiation as the only standard treatment. Recently, mutations in DMGs have arisen as potential therapeutic targets, specifically a mutation in one of the histone H3 genes, resulting in methionine substituted for lysine at site 27 (H3K27M). H3K27M induces a marked reduction in global acetylation of histone tails, altering chromatin structure and causing aberrant gene expression. Histone deacetylase inhibitors, HDACis, are epigenetic drugs th

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Jung, Jangham, Bohyeon Yu, and Aaron Diaz. "DNAR-15. GROUP 3 MEDULLOBLASTOMAS EXPLOIT A TRANSIENT MECHANISM OF TELOMERE REPAIR MEDIATED BY ZSCAN4 WHICH IS TARGETABLE FOR THERAPEUTIC BENEFIT WITH BRAIN-PENETRANT DRUGS." Neuro-Oncology 26, Supplement_8 (2024): viii120. http://dx.doi.org/10.1093/neuonc/noae165.0466.

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Abstract All cancers need some mechanism of telomere repair. However, it is unknown how Group 3 (G3) medulloblastomas (MB) repair their telomeres, even though MB is the most common malignant brain tumor in kids and G3 is its most aggressive subtype. With rare exceptions, G3 MBs lack telomerase gain-of-function alterations or evidence of constitutive alternative-lengthening-of-telomeres pathway activation. We profiled tumors from N=38 MB patients from UCSF via single-nucleus RNA sequencing; 13 cases were also subjected to single-cell assay for transposase-accessible chromatin by sequencing, and

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Janczura, Karolina J., Claude-Henry Volmar, Gregory C. Sartor, et al. "Inhibition of HDAC3 reverses Alzheimer’s disease-related pathologies in vitro and in the 3xTg-AD mouse model." Proceedings of the National Academy of Sciences 115, no. 47 (2018): E11148—E11157. http://dx.doi.org/10.1073/pnas.1805436115.

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Alzheimer’s disease (AD) is the leading cause of age-related dementia. Neuropathological hallmarks of AD include brain deposition of β-amyloid (Aβ) plaques and accumulation of both hyperphosphorylated and acetylated tau. RGFP-966, a brain-penetrant and selective HDAC3 inhibitor, or HDAC3 silencing, increases BDNF expression, increases histone H3 and H4 acetylation, decreases tau phosphorylation and tau acetylation at disease-associated sites, reduces β-secretase cleavage of the amyloid precursor protein (APP), and decreases Aβ1–42 accumulation in HEK-293 cells overexpressing APP with the doubl

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Parthasarathy, Akhila, Marc Garcia Moure, Jiasen He, et al. "EXTH-34. ACETYLATION SUPPRESSION MEETS ONCOLYTIC VIRUSES FOR THE TREATMENT OF PEDIATRIC DIFFUSE MIDLINE GLIOMA." Neuro-Oncology 26, Supplement_8 (2024): viii244. http://dx.doi.org/10.1093/neuonc/noae165.0965.

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Abstract Diffuse midline glioma (DMG) remains a devastating pediatric brain tumor without effective treatment. In a recent clinical trial, we demonstrated the feasibility and efficacy of Delta-24-RGD oncolytic virus combined with radiation therapy in patients with newly diagnosed diffuse intrinsic pontine gliomas (NCT03178032). Because the adenoviral protein E1A binds to P300 and redirects acetylation upon virus infection, we hypothesized that combining oncolytic adenoviruses with P300 inhibitors will cause a remarkable shifting in acetylation and the post-translational landscape of DMG, ultim

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Drzewiecka, Małgorzata, Dominika Jaśniak, Gabriela Barszczewska-Pietraszek, et al. "Class I HDAC Inhibition Leads to a Downregulation of FANCD2 and RAD51, and the Eradication of Glioblastoma Cells." Journal of Personalized Medicine 13, no. 9 (2023): 1315. http://dx.doi.org/10.3390/jpm13091315.

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HDAC inhibitors (HDACi) hold great potential as anticancer therapies due to their ability to regulate the acetylation of both histone and non-histone proteins, which is frequently disrupted in cancer and contributes to the development and advancement of the disease. Additionally, HDACi have been shown to enhance the cytotoxic effects of DNA-damaging agents such as radiation and cisplatin. In this study, we found that histone deacetylase inhibits valproic acid (VPA), synergized with PARP1 inhibitor (PARPi), talazoparib (BMN-673), and alkylating agent, and temozolomide (TMZ) to induce DNA damage

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Olufemi, Asuku Abraham, Ayinla Maryam Tayo, Ajibare Ayodeji Johnson, Adeyemo Michael Bolaji, Adeyemo Racheal Oluremi, and Olajide Tobiloba Samuel. "The Mechanisms of Melatonin’s Regulatory Functions on Neural Stem Cells’ Survival, Proliferation and Differentiation." JOURNAL OF BIOLOGY AND GENETIC RESEARCH 8, no. 2 (2023): 50–65. http://dx.doi.org/10.56201/jbgr.v8.no2.2022.pg50.65.

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Neural stem cells (NSCs) are cells that can self-replicate and differentiate in the central nervous system into neurons and glial cells. The sub granular zone (SGZ) in the hippocampal dentate gyrus (DG) and the sub ventricular zone (SVZ) are the two principal locations where NSCs are discovered in the adult brain. The recent identification of NSCs in adult mammalian brains has sparked a flurry of preclinical and translational research to examine brand-new strategies for treating neurodegenerative illnesses. Therefore, mobilizing endogenous NSCs has become a possible therapeutic strategy for br

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Nohesara, Shabnam, Hamid Mostafavi Abdolmaleky, and Sam Thiagalingam. "Potential for New Therapeutic Approaches by Targeting Lactate and pH Mediated Epigenetic Dysregulation in Major Mental Diseases." Biomedicines 12, no. 2 (2024): 457. http://dx.doi.org/10.3390/biomedicines12020457.

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Multiple lines of evidence have shown that lactate-mediated pH alterations in the brains of patients with neuropsychiatric diseases such as schizophrenia (SCZ), Alzheimer’s disease (AD) and autism may be attributed to mitochondrial dysfunction and changes in energy metabolism. While neuronal activity is associated with reduction in brain pH, astrocytes are responsible for rebalancing the pH to maintain the equilibrium. As lactate level is the main determinant of brain pH, neuronal activities are impacted by pH changes due to the binding of protons (H+) to various types of proteins, altering th

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Adamski, Jill, Zhendong Ma, Susan Nozell та Etty N. Benveniste. "17β-Estradiol Inhibits Class II Major Histocompatibility Complex (MHC) Expression: Influence on Histone Modifications and CBP Recruitment to the Class II MHC Promoter". Molecular Endocrinology 18, № 8 (2004): 1963–74. http://dx.doi.org/10.1210/me.2004-0098.

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Abstract Major histocompatibility complex (MHC) class II proteins are important for the initiation of immune responses and are essential for specific recognition of foreign antigens by the immune system. Regulation of class II MHC expression primarily occurs at the transcriptional level. The class II transactivator protein is the master regulator that is essential for both constitutive and interferon-γ-inducible class II MHC expression. Estrogen [17β-estradiol (17β-E2)] has been shown to have immunomodulatory effects. In this study, we show that 17β-E2 down-regulates interferon-γ inducible cla

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Perez, T., R. Berges, H. Maccario, D. Braguer, and S. Honoré. "P11.06 Non epigenetic effect of vorinostat in glioblastoma cells." Neuro-Oncology 21, Supplement_3 (2019): iii43. http://dx.doi.org/10.1093/neuonc/noz126.152.

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Abstract BACKGROUND Glioblastoma multiform (GBM) is the most frequent primitive brain tumor. GBM has a high recurrence and mortality. Histone deacetylase (HDAC) inhibitors have evoked great interest because they are able to change transcriptomic profiles to promote tumor cell death but also show undesirable side effects due to the lack of selectivity.We show new properties of low dose vorinostat, which inhibits cytoplasmic HDAC6 and display interesting non-epigenetics effects, especially on the microtubular cytoskeleton. MATERIAL AND METHODS We used murine (GL261) and human (U87 and GBM6 stem

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Krishna, Smriti Murali, Alexandra Fay Trollope, and Jonathan Golledge. "The relevance of epigenetics to occlusive cerebral and peripheral arterial disease." Clinical Science 128, no. 9 (2015): 537–58. http://dx.doi.org/10.1042/cs20140491.

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Athero-thrombosis of the arteries supplying the brain and lower limb are the main causes of stroke and limb loss. New therapies are needed to improve the outcomes of athero-thrombosis. Recent evidence suggests a role for epigenetic changes in the development and progression of ischaemic injury due to atherosclerotic occlusion of peripheral arteries. DNA hypermethylation have been associated with cardiovascular diseases. Histone post-translational modifications have also been implicated in atherosclerosis. Oxidized low-density lipoprotein regulated pro-inflammatory gene expression within endoth

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Ciafrè, Stefania, Valentina Carito, Giampiero Ferraguti, et al. "How alcohol drinking affects our genes: an epigenetic point of view." Biochemistry and Cell Biology 97, no. 4 (2019): 345–56. http://dx.doi.org/10.1139/bcb-2018-0248.

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This work highlights recent studies in epigenetic mechanisms that play a role in alcoholism, which is a complex multifactorial disorder. There is a large body of evidence showing that alcohol can modify gene expression through epigenetic processes, namely DNA methylation and nucleosomal remodeling via histone modifications. In that regard, chronic exposure to ethanol modifies DNA and histone methylation, histone acetylation, and microRNA expression. The alcohol-mediated chromatin remodeling in the brain promotes the transition from use to abuse and addiction. Unravelling the multiplex pattern

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Lilja, Tobias, Nina Heldring, and Ola Hermanson. "Like a rolling histone: Epigenetic regulation of neural stem cells and brain development by factors controlling histone acetylation and methylation." Biochimica et Biophysica Acta (BBA) - General Subjects 1830, no. 2 (2013): 2354–60. http://dx.doi.org/10.1016/j.bbagen.2012.08.011.

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Fock, Ekaterina, and Rimma Parnova. "Mechanisms of Blood–Brain Barrier Protection by Microbiota-Derived Short-Chain Fatty Acids." Cells 12, no. 4 (2023): 657. http://dx.doi.org/10.3390/cells12040657.

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Impairment of the blood–brain barrier (BBB) integrity is implicated in the numerous neurological disorders associated with neuroinflammation, neurodegeneration and aging. It is now evident that short-chain fatty acids (SCFAs), mainly acetate, butyrate and propionate, produced by anaerobic bacterial fermentation of the dietary fiber in the intestine, have a key role in the communication between the gastrointestinal tract and nervous system and are critically important for the preservation of the BBB integrity under different pathological conditions. The effect of SCFAs on the improvement of the

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Murray, Elaine K., Annie Hien, Geert J. de Vries, and Nancy G. Forger. "Epigenetic Control of Sexual Differentiation of the Bed Nucleus of the Stria Terminalis." Endocrinology 150, no. 9 (2009): 4241–47. http://dx.doi.org/10.1210/en.2009-0458.

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Abstract The principal nucleus of the bed nucleus of the stria terminalis (BNSTp) is larger in volume and contains more cells in male than female mice. These sex differences depend on testosterone and arise from a higher rate of cell death during early postnatal life in females. There is a delay of several days between the testosterone surge at birth and sexually dimorphic cell death in the BNSTp, suggesting that epigenetic mechanisms may be involved. We tested the hypothesis that chromatin remodeling plays a role in sexual differentiation of the BNSTp by manipulating the balance between histo

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Farrelly, Lorna, Shuangping Zhang, Erin Flaherty, et al. "T9. EPIGENETIC PROFILING IN SCHIZOPHRENIA DERIVED HUMAN INDUCED PLURIPOTENT STEM CELLS (HIPSCS) AND NEURONS." Schizophrenia Bulletin 46, Supplement_1 (2020): S234. http://dx.doi.org/10.1093/schbul/sbaa029.569.

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Abstract Background Schizophrenia (SCZ) is a severe psychiatric disorder affecting ~1% of the world’s population. It is largely heritable with genetic risk reflected by a combination of common variants of small effect and highly penetrant rare mutations. Chromatin modifications are known to play critical roles in the mediation of many neurodevelopmental processes, and, when disturbed, may also contribute to the precipitation of psychiatric disorders, such as SCZ. While a handful of candidate-based studies have measured changes in promoter-bound histone modifications, few mechanistic studies ha

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Denver, Robert J., and Keith E. Williamson. "Identification of a Thyroid Hormone Response Element in the Mouse Krüppel-Like Factor 9 Gene to Explain Its Postnatal Expression in the Brain." Endocrinology 150, no. 8 (2009): 3935–43. http://dx.doi.org/10.1210/en.2009-0050.

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Brain development is critically dependent on thyroid hormone (T3). Krüppel-like factor 9 (Klf9) is a T3-inducible gene in developing rat brain, and several lines of evidence support that KLF9 plays a key role in neuronal morphogenesis. Here we extend our findings to the mouse and demonstrate the presence of a functional T3 response element (T3RE) in the 5′ flanking region of the mouse Klf9 gene. Klf9 mRNA is strongly induced in the mouse hippocampus and cerebellum in a developmental stage- and T3-dependent manner. Computer analysis identified a near optimal direct repeat 4 (DR-4) T3RE 3.8 kb

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Hashizume, Rintaro. "IL-5 EPIGENETIC REGULATION IN GLIOMA METABOLISM." Neuro-Oncology Advances 6, Supplement_4 (2024): iv28. http://dx.doi.org/10.1093/noajnl/vdae173.111.

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Abstract In most cancer cells including glioma cells, glucose is at-least partially metabolized to lactate through the Warburg Effect, which refers to the non-oxidative metabolism of glucose even in the presence of sufficient oxygen. In addition to the advantage conferred upon glioma cells by the canonical glycolysis pathway, through supporting rapid proliferation and survival, its end product, lactate, serves as a key factor to regulate H3K27 acetylation (H3K27ac) through histone deacetylases (HDACs). We and others have shown that increase lactate metabolism related to tumor progression in hi

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Kitange, Gaspar J., Danielle M. Burgenske, Katrina K. Bakken, et al. "EXTH-12. INHIBITION OF CBP/p300 HISTONE ACETYLATION ACTIVITY ENHANCES TEMOZOLOMIDE ACTIVITY IN GLIOBLASTOMA PATIENT DERIVED XENOGRAFTS." Neuro-Oncology 22, Supplement_2 (2020): ii89. http://dx.doi.org/10.1093/neuonc/noaa215.366.

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Abstract There is an unmet need to identify novel targets that can sensitize temozolomide (TMZ) or prevent resistance in GBM. We have demonstrated that retinoblastoma binding protein 4 (RBBP4) interacts with p300 to modulate expression of genes involved in homologous recombination (HR), including RAD51. In vitro, RBBP4- or p300-shRNA significantly sensitized TMZ in patient derived xenograft (PDX) GBM43 cells (relative fluorescence for 100µM TMZ treated control shNT cells was 0.89 ± 0.1 vs 0.47± 0.09 and 0.39 ± 0.01 for shRBBP4 and shp300, respectively (p&lt; 0.01)). TMZ sensitization incre

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Kim, Su-Bin, Jong-Ik Heo, Hyunggee Kim та Kwang Seok Kim. "Acetylation of PGC1α by Histone Deacetylase 1 Downregulation Is Implicated in Radiation-Induced Senescence of Brain Endothelial Cells". Journals of Gerontology: Series A 74, № 6 (2018): 787–93. http://dx.doi.org/10.1093/gerona/gly167.

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YAVUZ, Selda, and Onur BAYKARA. "An Epigenetic Insight Into the Gliomas." Annals of Medical Research 30, no. 7 (2023): 1. http://dx.doi.org/10.5455/annalsmedres.2023.07.154.

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Glioma is one of the most aggressive tumors that develop in the glial cells of the brain. It has subtypes such as astrocytomas, oligodendrogliomas and ependymomas. Gliomas comprise about 30% of all brain tumors and are mostly malignant. Gliomas are classified into four grades and the severity of the disease increases with the grade. Like many cancer types, development of gliomas is under the control of genetic, epigenetic and environmental factors. Epigenetics is the area that examines the expression changes in genes that do not change the structure of DNA, but cause behavioral changes in unco

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Liu, Yingzi, Xiaoyang Duan, Chunyan Zhang, et al. "KAT6B May Be Applied as a Potential Therapeutic Target for Glioma." Journal of Oncology 2022 (April 6, 2022): 1–10. http://dx.doi.org/10.1155/2022/2500092.

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Glioma is a prevalent malignancy among brain tumors with high modality and low prognosis. Ferroptosis has been identified to play a crucial role in the progression and treatment of cancers. KAT6B, as a histone acetyltransferase, is involved in multiple cancer development. However, the function of KAT6B in glioma is still elusive. Here, we aimed to evaluate the effect of KAT6B on ferroptosis in glioma cells and explored the potential mechanisms. We observed that the expression of KAT6B was enhanced in clinical glioma samples. The viability of glioma cells was repressed by erastin and the overex

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Chandler, Ms Rebecca, Dr Jane Alder, Dr Roshini Mathews, and Dr Izabela Stasik. "INVESTIGATING CUDC-101 EFFECT AND MECHANISM OF ACTION AGAINST GLIOBLASTOMA IN VITRO." Neuro-Oncology 26, Supplement_7 (2024): vii16. http://dx.doi.org/10.1093/neuonc/noae158.062.

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Abstract AIMS Glioblastoma (GB) has complex pathophysiology, diﬃcult treatment and resultant poor prognosis. Its median survival rate is approximately 15 months. The aggressive nature of GB results in rapid disease progression in 60-70% patients often within 12 weeks. Limited treatment options include maximal safe surgical resection, followed by radiotherapy and temozolomide (TMZ). The blood brain barrier restricts chemotherapeutic entry and increases dosage leading to increased side effects and decreased treatment tolerance. Furthermore, signiﬁcant disease heterogeneity means reoccurrence is

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Van Roy, Zachary, and Tammy L. Kielian. "Epigenetic changes program innate immunity during Staphylococcus aureuscraniotomy infection." Journal of Immunology 210, no. 1_Supplement (2023): 148.04. http://dx.doi.org/10.4049/jimmunol.210.supp.148.04.

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Abstract A craniotomy is performed to access the brain for the treatment of tumors, epilepsy, or hemorrhage. Despite advances in surgical techniques, infections occur in 1–3% of cases, half of which are caused by Staphylococcus aureus(S. aureus). Since epigenetic mechanisms are critical for regulating leukocyte activation, we examined whether S. aureusdrives epigenetic modifications to regulate immune cell function during craniotomy infection. A high-throughput screen of an epigenetic compound library using primary mouse microglia identified BET protein family members and histone deacetylases

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Chang, Hui Hua, Yao-Yuan Chang, Bing-Chen Tsai, et al. "A Selective Histone Deacetylase Inhibitor Induces Autophagy and Cell Death via SCNN1A Downregulation in Glioblastoma Cells." Cancers 14, no. 18 (2022): 4537. http://dx.doi.org/10.3390/cancers14184537.

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Glioblastoma multiforme (GBM) is a grade IV, highly malignant brain tumor. Because of the heterogeneity of GBM, a multitarget drug is a rational strategy for GBM treatment. Histone deacetylase inhibitors (HDACis) regulate the expression of numerous genes involved in cell death, apoptosis, and tumorigenesis. We found that the HDAC4/HDAC5 inhibitor LMK235 at 0.5 µM significantly reduced the cell viability and colony formation of patient-derived, temozolomide-resistant GBM P#5 TMZ-R, U-87 MG, and T98G cells. Moreover, LMK235 also significantly increased TUBA acetylation, which is an indicator of

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Ma, Shuangping, Lei Wang, Junhe Zhang, Lujing Geng, and Junzheng Yang. "The role of transcriptional and epigenetic modifications in astrogliogenesis." PeerJ 12 (September 20, 2024): e18151. http://dx.doi.org/10.7717/peerj.18151.

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Astrocytes are widely distributed and play a critical role in the central nervous system (CNS) of the human brain. During the development of CNS, astrocytes provide essential nutritional and supportive functions for neural cells and are involved in their metabolism and pathological processes. Despite the numerous studies that have reported on the regulation of astrogliogenesis at the transcriptional and epigenetic levels, there is a paucity of literature that provides a comprehensive summary of the key factors influencing this process. In this review, we analyzed the impact of transcription fa

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Ehteda, Anahid, Sandy Simon, Laura Franshaw, et al. "HGG-09. TARGETING FACILITATES CHROMATIN TRANSCRIPTION (FACT) AS A NOVEL STRATEGY THAT ENHANCES RESPONSE TO HISTONE DEACETYLASE (HDAC) INHIBITION IN DIPG." Neuro-Oncology 23, Supplement_1 (2021): i18—i19. http://dx.doi.org/10.1093/neuonc/noab090.075.

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Abstract DIPG is an aggressive and incurable childhood brain tumour for which new treatments are needed. A high throughput drug screen of 3500 pharmaceutical compounds identified anti-malarials, including quinacrine as having potent activity against DIPG neurospheres. CBL0137, a compound modelled on quinacrine, is a novel anti-cancer compound which targets Facilitates Chromatin Transcription (FACT), a chromatin remodelling complex involved in transcription, replication, and DNA repair. CBL0137 effectively crosses the blood-brain barrier and has recently completed Phase I testing in adult patie

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Cabrera, Omar Hoseá, Nemanja Useinovic, and Vesna Jevtovic-Todorovic. "Neonatal anesthesia and dysregulation of the epigenome." Biology of Reproduction 105, no. 3 (2021): 720–34. http://dx.doi.org/10.1093/biolre/ioab136.

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Abstract Each year, millions of infants and children are anesthetized for medical and surgical procedures. Yet, a substantial body of preclinical evidence suggests that anesthetics are neurotoxins that cause rapid and widespread apoptotic cell death in the brains of infant rodents and nonhuman primates. These animals have persistent impairments in cognition and behavior many weeks or months after anesthesia exposure, leading us to hypothesize that anesthetics do more than simply kill brain cells. Indeed, anesthetics cause chronic neuropathology in neurons that survive the insult, which then in

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You, Dahea, Xia Wen, Ludwik Gorczyca, Ayeshia Morris, Jason R. Richardson, and Lauren M. Aleksunes. "Increased MDR1 Transporter Expression in Human Brain Endothelial Cells Through Enhanced Histone Acetylation and Activation of Aryl Hydrocarbon Receptor Signaling." Molecular Neurobiology 56, no. 10 (2019): 6986–7002. http://dx.doi.org/10.1007/s12035-019-1565-7.

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Lossi, Laura, Claudia Castagna, and Adalberto Merighi. "An Overview of the Epigenetic Modifications in the Brain under Normal and Pathological Conditions." International Journal of Molecular Sciences 25, no. 7 (2024): 3881. http://dx.doi.org/10.3390/ijms25073881.

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Epigenetic changes are changes in gene expression that do not involve alterations to the DNA sequence. These changes lead to establishing a so-called epigenetic code that dictates which and when genes are activated, thus orchestrating gene regulation and playing a central role in development, health, and disease. The brain, being mostly formed by cells that do not undergo a renewal process throughout life, is highly prone to the risk of alterations leading to neuronal death and neurodegenerative disorders, mainly at a late age. Here, we review the main epigenetic modifications that have been d

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Torrini, Consuelo, Trang Nguyen, Chang Shu, et al. "ETMM-05. LACTIC ACID FACILITATES GLIOBLASTOMA GROWTH THROUGH MODULATION OF THE EPIGENOME." Neuro-Oncology Advances 3, Supplement_1 (2021): i15. http://dx.doi.org/10.1093/noajnl/vdab024.061.

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Abstract Glioblastoma (GBM) is the most common primary malignant brain tumor with an unfavorable prognosis. While GBMs utilize glucose, there are other carbon sources at their disposal. Lactate accumulates to a significant amount in the infiltrative margin of GBMs. In the current study, we demonstrated that lactate rescued patient-derived xenograft (PDX) GBM cells from nutrient deprivation mediated cell death and inhibition of growth. Transcriptome analysis, ATAC-seq and CHIP-seq. showed that lactic acid exposure entertained a signature of cell cycle progression and oxidative phosphorylation (

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Jankowska-Kulawy, Agnieszka, Joanna Klimaszewska-Łata, Sylwia Gul-Hinc, Anna Ronowska, and Andrzej Szutowicz. "Metabolic and Cellular Compartments of Acetyl-CoA in the Healthy and Diseased Brain." International Journal of Molecular Sciences 23, no. 17 (2022): 10073. http://dx.doi.org/10.3390/ijms231710073.

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The human brain is characterised by the most diverse morphological, metabolic and functional structure among all body tissues. This is due to the existence of diverse neurons secreting various neurotransmitters and mutually modulating their own activity through thousands of pre- and postsynaptic interconnections in each neuron. Astroglial, microglial and oligodendroglial cells and neurons reciprocally regulate the metabolism of key energy substrates, thereby exerting several neuroprotective, neurotoxic and regulatory effects on neuronal viability and neurotransmitter functions. Maintenance of

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Kataoka, Shunsuke, Kazuhiro Takuma, Yuta Hara, Yuko Maeda, Yukio Ago, and Toshio Matsuda. "Autism-like behaviours with transient histone hyperacetylation in mice treated prenatally with valproic acid." International Journal of Neuropsychopharmacology 16, no. 1 (2013): 91–103. http://dx.doi.org/10.1017/s1461145711001714.

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Abstract Maternal use of valproic acid (VPA) during pregnancy has been implicated in the aetiology of autism spectrum disorders in children, and rodents prenatally exposed to VPA showed behavioural alterations similar to those observed in humans with autism. However, the exact mechanism for VPA-induced behavioural alterations is not known. To study this point, we examined the effects of prenatal exposure to VPA and valpromide, a VPA analog lacking histone deacetylase inhibition activity, on behaviours, cortical pathology and histone acetylation levels in mice. Mice exposed to VPA at embryonic

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Torrini, Consuelo, Trang Nguyen, Chang Shu, et al. "EPCO-16. LACTIC ACID IS AN EPIGENETIC METABOLITE THAT DRIVES GLIOBLASTOMA SURVIVAL AND GROWTH." Neuro-Oncology 22, Supplement_2 (2020): ii72. http://dx.doi.org/10.1093/neuonc/noaa215.295.

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Abstract Glioblastoma (GBM) is the most common primary malignant brain tumor with an unfavorable prognosis and a reprogrammed metabolism. While tumors utilize glucose, there are other carbon sources at their disposal. Originally considered as a waste product of glucose catabolism, lactate accumulates to a significant amount in tumor tissue. We launched our studies with the central hypothesis that lactate is metabolized by GBM cells to promote their survival via modulation of the epigenome. We showed that lactate rescued patient-derived xenograft (PDX) GBM cells from nutrient deprivation mediat

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Verma, Pratibha, Omshree Shetty, Sweta Parab, Karen Menezes, and Priyanka Parte. "Developmental Testicular Expression, Cloning, and Characterization of Rat HDAC6 In Silico." BioMed Research International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/5170680.

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We had previously reported presence of histone deacetylase 6 (HDAC6) in sperm and demonstrated its tubulin deacetylase activity and role in sperm motility in rat. In the present study we report its abundant expression in testis, epididymis, accessory sex organs, brain, and adrenal. In the testis, HDAC6 transcript and protein were observed throughout development. We therefore cloned the gene from rat testis using primers for hdac6 (accession number XM_228753.8) in order to determine the role of acetylation/deacetylation in spermatogenesis. The cloned rat hdac6 gene is ~3.5 kb with 28 exons and

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Morland, Cecilie, Anne-Sofie Frøland, Mi Nguyen Pettersen, et al. "Propionate enters GABAergic neurons, inhibits GABA transaminase, causes GABA accumulation and lethargy in a model of propionic acidemia." Biochemical Journal 475, no. 4 (2018): 749–58. http://dx.doi.org/10.1042/bcj20170814.

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Propionic acidemia is the accumulation of propionate in blood due to dysfunction of propionyl-CoA carboxylase. The condition causes lethargy and striatal degeneration with motor impairment in humans. How propionate exerts its toxic effect is unclear. Here, we show that intravenous administration of propionate causes dose-dependent propionate accumulation in the brain and transient lethargy in mice. Propionate, an inhibitor of histone deacetylase, entered GABAergic neurons, as could be seen from increased neuronal histone H4 acetylation in the striatum and neocortex. Propionate caused an increa

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Liu, Juan, Xiang Zhou, Qing Li, et al. "Role of Phosphorylated HDAC4 in Stroke-Induced Angiogenesis." BioMed Research International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/2957538.

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Acetylation or deacetylation of chromatin proteins and transcription factors is part of a complex signaling system that is involved in the control of neurological disorders. Recent studies have demonstrated that histone deacetylases (HDACs) exert protective effects in attenuating neuronal injury after ischemic insults. Class IIa HDAC4 is highly expressed in the brain, and neuronal activity depends on the nucleocytoplasmic shuttling of HDAC4. However, little is known about HDAC4 and its roles in ischemic stroke. In this study, we report that phosphorylation of HDAC4 was remarkably upregulated a

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Nguyen, Thi T., Kyucheol Cho, Sabrina A. Stratton, and Michelle Craig Barton. "Transcription Factor Interactions and Chromatin Modifications Associated with p53-Mediated, Developmental Repression of the Alpha-Fetoprotein Gene." Molecular and Cellular Biology 25, no. 6 (2005): 2147–57. http://dx.doi.org/10.1128/mcb.25.6.2147-2157.2005.

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ABSTRACT We performed chromatin immunoprecipitation (ChIP) analyses of developmentally staged solid tissues isolated from wild-type and p53-null mice to determine specific histone N-terminal modifications, histone-modifying proteins, and transcription factor interactions at the developmental repressor region (−850) and core promoter of the hepatic tumor marker alpha-fetoprotein (AFP) gene. Both repression of AFP during liver development and silencing in the brain, where AFP is never expressed, are associated with dimethylation of histone H3 lysine 9 (DiMetH3K9) and the presence of heterochroma

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Ramirez, Lorimar, Melissa Singh, and Joya Chandra. "HDAC and LSD1 Inhibitors Synergize to Induce Cell Death in Acute Leukemia Cells." Blood 118, no. 21 (2011): 1427. http://dx.doi.org/10.1182/blood.v118.21.1427.1427.

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Abstract Abstract 1427 Histone deacetylase inhibitors (HDACi) are a class of emerging epigenetic therapies which are being used to treat cancer. Two HDACi (vorinostat and romidepsin) are FDA approved for cutaneous T-cell lymphoma. HDACi have been employed in clinical trials for acute leukemia, but single agent activity has been limited. Improved efficacy is observed when combined with other anticancer agents. In the current study we addressed acute leukemia models using vorinostat, a pan-HDACi that inhibits HDAC class I, II, and IV and entinostat, a newer HDACi that inhibits HDAC class I more

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