| Literature DB >> 15885809 |
Sandra Camelo1, Antonio H Iglesias, Daehee Hwang, Brice Due, Hoon Ryu, Karen Smith, Steven G Gray, Jaime Imitola, German Duran, Basel Assaf, Brett Langley, Samia J Khoury, George Stephanopoulos, Umberto De Girolami, Rajiv R Ratan, Robert J Ferrante, Fernando Dangond.
Abstract
We demonstrate 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). TSA up-regulates antioxidant, anti-excitotoxicity and pro-neuronal growth and differentiation mRNAs. TSA also inhibits caspase activation and down-regulates gene targets of the pro-apoptotic E2F transcription factor pathway. In splenocytes, TSA reduces chemotactic, pro-Th1 and pro-proliferative mRNAs. A transcriptional imbalance in MS may contribute to immune dysregulation and neurodegeneration, and we identify HDAC inhibition as a transcriptional intervention to ameliorate this imbalance.Entities:
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Year: 2005 PMID： 15885809 DOI： 10.1016/j.jneuroim.2005.02.022
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478