Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis
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). T...
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| Veröffentlicht in: | Journal of neuroimmunology 2005-07, Vol.164 (1), p.10-21 |
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| creator | Camelo, Sandra Iglesias, Antonio H. Hwang, Daehee Due, Brice Ryu, Hoon Smith, Karen Gray, Steven G. Imitola, Jaime Duran, German Assaf, Basel Langley, Brett Khoury, Samia J. Stephanopoulos, George De Girolami, Umberto Ratan, Rajiv R. Ferrante, Robert J. Dangond, Fernando |
| description | 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. |
| doi_str_mv | 10.1016/j.jneuroim.2005.02.022 |
| format | Article |
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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.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/j.jneuroim.2005.02.022</identifier><identifier>PMID: 15885809</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Cell Death - drug effects ; Cells, Cultured ; Cerebral Cortex - cytology ; Cytokines - genetics ; Cytokines - metabolism ; Disease Models, Animal ; Drug Administration Schedule ; Drug Interactions ; Embryo, Mammalian ; Encephalomyelitis, Autoimmune, Experimental - chemically induced ; Encephalomyelitis, Autoimmune, Experimental - drug therapy ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Experimental autoimmune encephalomyelitis ; Female ; Gene Expression Profiling - methods ; Gene Expression Regulation - drug effects ; Glycoproteins ; Histone deacetylase ; Hydroxamic Acids - therapeutic use ; Immunohistochemistry - methods ; Mice ; Mice, Inbred C57BL ; Microarrays ; Multiple sclerosis ; Myelin-Oligodendrocyte Glycoprotein ; Neurons - drug effects ; Oligonucleotide Array Sequence Analysis - methods ; Peptide Fragments ; Protein Synthesis Inhibitors - therapeutic use ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - metabolism ; Severity of Illness Index ; Spleen - drug effects ; Spleen - metabolism ; Tetrazolium Salts ; Thiazoles ; Time Factors ; Trichostatin A</subject><ispartof>Journal of neuroimmunology, 2005-07, Vol.164 (1), p.10-21</ispartof><rights>2005 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-27cc02d51f728f19a2b7b7f83de7a2a5f74e9caf6aebef93762fc2eb9830774b3</citedby><cites>FETCH-LOGICAL-c428t-27cc02d51f728f19a2b7b7f83de7a2a5f74e9caf6aebef93762fc2eb9830774b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jneuroim.2005.02.022$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15885809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Camelo, Sandra</creatorcontrib><creatorcontrib>Iglesias, Antonio H.</creatorcontrib><creatorcontrib>Hwang, Daehee</creatorcontrib><creatorcontrib>Due, Brice</creatorcontrib><creatorcontrib>Ryu, Hoon</creatorcontrib><creatorcontrib>Smith, Karen</creatorcontrib><creatorcontrib>Gray, Steven G.</creatorcontrib><creatorcontrib>Imitola, Jaime</creatorcontrib><creatorcontrib>Duran, German</creatorcontrib><creatorcontrib>Assaf, Basel</creatorcontrib><creatorcontrib>Langley, Brett</creatorcontrib><creatorcontrib>Khoury, Samia J.</creatorcontrib><creatorcontrib>Stephanopoulos, George</creatorcontrib><creatorcontrib>De Girolami, Umberto</creatorcontrib><creatorcontrib>Ratan, Rajiv R.</creatorcontrib><creatorcontrib>Ferrante, Robert J.</creatorcontrib><creatorcontrib>Dangond, Fernando</creatorcontrib><title>Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>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.</description><subject>Animals</subject><subject>Cell Death - drug effects</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Drug Administration Schedule</subject><subject>Drug Interactions</subject><subject>Embryo, Mammalian</subject><subject>Encephalomyelitis, Autoimmune, Experimental - chemically induced</subject><subject>Encephalomyelitis, Autoimmune, Experimental - drug therapy</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Experimental autoimmune encephalomyelitis</subject><subject>Female</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glycoproteins</subject><subject>Histone deacetylase</subject><subject>Hydroxamic Acids - therapeutic use</subject><subject>Immunohistochemistry - methods</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microarrays</subject><subject>Multiple sclerosis</subject><subject>Myelin-Oligodendrocyte Glycoprotein</subject><subject>Neurons - drug effects</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>Peptide Fragments</subject><subject>Protein Synthesis Inhibitors - therapeutic use</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - metabolism</subject><subject>Severity of Illness Index</subject><subject>Spleen - drug effects</subject><subject>Spleen - metabolism</subject><subject>Tetrazolium Salts</subject><subject>Thiazoles</subject><subject>Time Factors</subject><subject>Trichostatin A</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1r3DAQhkVpaDZp_0LQqTdv9WGt5FtDaNpCIJfkLGR5hLXYkivJbfecPx4tu6XHwMAw8Mw7Hy9CN5RsKaG7L_vtPsCaop-3jBCxJawGe4c2VEnWqJbR92hTQdEIydQlusp5TwgVvO0-oEsqlBKKdBv08pRMyDb5pfgYzITLCMksB_zHl_FY4NHnEgPgAYyFcphMBuzD6HtfYsIleTvGXEzxAd9iM8PkYzIFMoa_CyQ_QyhV1qyl7jqvVQiChWU0U5wPFS4-f0QXzkwZPp3zNXq-__Z096N5ePz-8-72obEtU6Vh0lrCBkFdvcjRzrBe9tIpPoA0zAgnW-iscTsDPbiOyx1zlkHfKU6kbHt-jT6fdJcUf62Qi559tjBNJkBcs2aEccKVehOkkgvOlKzg7gTaFHNO4PRSLzbpoCnRR5_0Xv_zSR990oTVYLXx5jxh7WcY_redjanA1xMA9SG_PSSdrT9-bvAJbNFD9G_NeAUsz61P</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Camelo, Sandra</creator><creator>Iglesias, Antonio H.</creator><creator>Hwang, Daehee</creator><creator>Due, Brice</creator><creator>Ryu, Hoon</creator><creator>Smith, Karen</creator><creator>Gray, Steven G.</creator><creator>Imitola, Jaime</creator><creator>Duran, German</creator><creator>Assaf, Basel</creator><creator>Langley, Brett</creator><creator>Khoury, Samia J.</creator><creator>Stephanopoulos, George</creator><creator>De Girolami, Umberto</creator><creator>Ratan, Rajiv R.</creator><creator>Ferrante, Robert J.</creator><creator>Dangond, Fernando</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>7TM</scope></search><sort><creationdate>20050701</creationdate><title>Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis</title><author>Camelo, Sandra ; Iglesias, Antonio H. ; Hwang, Daehee ; Due, Brice ; Ryu, Hoon ; Smith, Karen ; Gray, Steven G. ; Imitola, Jaime ; Duran, German ; Assaf, Basel ; Langley, Brett ; Khoury, Samia J. ; Stephanopoulos, George ; De Girolami, Umberto ; Ratan, Rajiv R. ; Ferrante, Robert J. ; Dangond, Fernando</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-27cc02d51f728f19a2b7b7f83de7a2a5f74e9caf6aebef93762fc2eb9830774b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Cell Death - drug effects</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Drug Administration Schedule</topic><topic>Drug Interactions</topic><topic>Embryo, Mammalian</topic><topic>Encephalomyelitis, Autoimmune, Experimental - chemically induced</topic><topic>Encephalomyelitis, Autoimmune, Experimental - drug therapy</topic><topic>Encephalomyelitis, Autoimmune, Experimental - genetics</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Experimental autoimmune encephalomyelitis</topic><topic>Female</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glycoproteins</topic><topic>Histone deacetylase</topic><topic>Hydroxamic Acids - therapeutic use</topic><topic>Immunohistochemistry - methods</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microarrays</topic><topic>Multiple sclerosis</topic><topic>Myelin-Oligodendrocyte Glycoprotein</topic><topic>Neurons - drug effects</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>Peptide Fragments</topic><topic>Protein Synthesis Inhibitors - therapeutic use</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - metabolism</topic><topic>Severity of Illness Index</topic><topic>Spleen - drug effects</topic><topic>Spleen - metabolism</topic><topic>Tetrazolium Salts</topic><topic>Thiazoles</topic><topic>Time Factors</topic><topic>Trichostatin A</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Camelo, Sandra</creatorcontrib><creatorcontrib>Iglesias, Antonio H.</creatorcontrib><creatorcontrib>Hwang, Daehee</creatorcontrib><creatorcontrib>Due, Brice</creatorcontrib><creatorcontrib>Ryu, Hoon</creatorcontrib><creatorcontrib>Smith, Karen</creatorcontrib><creatorcontrib>Gray, Steven G.</creatorcontrib><creatorcontrib>Imitola, Jaime</creatorcontrib><creatorcontrib>Duran, German</creatorcontrib><creatorcontrib>Assaf, Basel</creatorcontrib><creatorcontrib>Langley, Brett</creatorcontrib><creatorcontrib>Khoury, Samia J.</creatorcontrib><creatorcontrib>Stephanopoulos, George</creatorcontrib><creatorcontrib>De Girolami, Umberto</creatorcontrib><creatorcontrib>Ratan, Rajiv R.</creatorcontrib><creatorcontrib>Ferrante, Robert J.</creatorcontrib><creatorcontrib>Dangond, Fernando</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Camelo, Sandra</au><au>Iglesias, Antonio H.</au><au>Hwang, Daehee</au><au>Due, Brice</au><au>Ryu, Hoon</au><au>Smith, Karen</au><au>Gray, Steven G.</au><au>Imitola, Jaime</au><au>Duran, German</au><au>Assaf, Basel</au><au>Langley, Brett</au><au>Khoury, Samia J.</au><au>Stephanopoulos, George</au><au>De Girolami, Umberto</au><au>Ratan, Rajiv R.</au><au>Ferrante, Robert J.</au><au>Dangond, Fernando</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>164</volume><issue>1</issue><spage>10</spage><epage>21</epage><pages>10-21</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><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.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>15885809</pmid><doi>10.1016/j.jneuroim.2005.02.022</doi><tpages>12</tpages></addata></record> |
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| ispartof | Journal of neuroimmunology, 2005-07, Vol.164 (1), p.10-21 |
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| subjects | Animals Cell Death - drug effects Cells, Cultured Cerebral Cortex - cytology Cytokines - genetics Cytokines - metabolism Disease Models, Animal Drug Administration Schedule Drug Interactions Embryo, Mammalian Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - drug therapy Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - pathology Experimental autoimmune encephalomyelitis Female Gene Expression Profiling - methods Gene Expression Regulation - drug effects Glycoproteins Histone deacetylase Hydroxamic Acids - therapeutic use Immunohistochemistry - methods Mice Mice, Inbred C57BL Microarrays Multiple sclerosis Myelin-Oligodendrocyte Glycoprotein Neurons - drug effects Oligonucleotide Array Sequence Analysis - methods Peptide Fragments Protein Synthesis Inhibitors - therapeutic use Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - metabolism Severity of Illness Index Spleen - drug effects Spleen - metabolism Tetrazolium Salts Thiazoles Time Factors Trichostatin A |
| title | Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis |
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