Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis.
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Summary
It is demonstrated that the histone deacetylase (HDAC) inhibitor drug trichostatin A (TSA) reduces spinal cord inflammation, demyelination, neuronal and axonal loss and ameliorates disability in the relapsing phase of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS).
- Type
- article
- Published
- 2005-07-01
- Cited by
- 278
- References
- 58
- OpenAlex
- https://openalex.org/W2011718960
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:46086446
Keywords
Trichostatin A, Experimental autoimmune encephalomyelitis, Histone deacetylase, Histone deacetylase inhibitor, Neurodegeneration
References
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- Insulin-Like Growth Factor (IGF) Signaling through Type 1 IGF Receptor Plays an Important Role in Remyelination
- Sp1 and Sp3 Are Oxidative Stress-Inducible, Antideath Transcription Factors in Cortical Neurons
- The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses
- Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease
- Chemokine Upregulation Follows Cytokine Expression in Chronic Relapsing Experimental Autoimmune Encephalomyelitis
- Regulation of neuronal traits by a novel transcriptional complex.
- The Regulation of Reactive Oxygen Species Production during Programmed Cell Death
- Identification of novel E2F1-regulated genes by microarray.
- Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions
- The HMG-CoA reductase inhibitor, atorvastatin, promotes a Th2 bias and reverses paralysis in central nervous system autoimmune disease
- Glutathione Peroxidase Protects against Peroxynitrite-mediated Oxidations
- Phosphatidylinositol 3-kinase couples the interleukin-2 receptor to the cell cycle regulator E2F.
- Glutathione deficiency leads to mitochondrial damage in brain.
- Insights into glutamate transport regulation in human astrocytes: Cloning of the promoter for excitatory amino acid transporter 2 (EAAT2)
Cited by
- HDAC inhibitors as anti‐inflammatory agents
- Development of histone deacetylase inhibitors for cancer treatment
- Differential effects of selective HDAC inhibitors on macrophage inflammatory responses to the Toll‐like receptor 4 agonist LPS
- 4-iodophenyl isothiocyanate: A neuroprotective compound
- Histone deacetylase inhibition activates transcription factor Nrf2 and protects against cerebral ischemic damage
- Epigenetics in sepsis: targeting histone deacetylases.
- Prospects for epigenetic compounds in the treatment of autoimmune disease.
- Histone Deacetylase Inhibitors as Therapeutic Agents for Acute Central Nervous System Injuries
- Rationale for HDAC inhibitor therapy in autoimmunity and transplantation.
- Regulierung der Funktion Dendritischer Zellen durch Histon-Deacetylase-Inhibitoren
- Role of epigenetics in inflammation-associated diseases.
- Creating a Pro-survival and Anti-inflammatory Phenotype by Modulation of Acetylation in Models of Hemorrhagic and Septic Shock
- Apicidin, the Histone Deacetylase Inhibitor, Suppresses TH1 Polarization of Murine Bone Marrow-Derived Dendritic Cells
- Histone Deacetylase (HDAC) Inhibition as a Novel Treatment for Diabetes Mellitus
- Transcriptional regulatory mechanisms involved in CYP46A1 up-regulation by histone deacetylase inhibitors:from chromatin structure to transcription factors
- Targeting histone deacetylases for the treatment of immune, endocrine & metabolic disorders.
- Nutrients and Epigenetics
- HDAC inhibition as a therapeutic potential to treat metabolic diseases
- Metabolism and epigenetics in the nervous system: Creating cellular fitness and resistance to neuronal death in neurological conditions via modulation of oxygen-, iron-, and 2-oxoglutarate-dependent dioxygenases
- n‐Butyrate Anergized Effector CD4+ T Cells Independent of Regulatory T cell Generation or Activity
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