Tonicity-responsive enhancer binding protein haplodeficiency attenuates seizure severity and NF-κB-mediated neuroinflammation in kainic acid-induced seizures
Kainic acid (KA)-induced seizures followed by neuronal death are associated with neuroinflammation and blood–brain barrier (BBB) leakage. Tonicity-responsive enhancer binding protein (TonEBP) is known as a transcriptional factor activating osmoprotective genes, and in brain, it is expressed in neuro...
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| Veröffentlicht in: | Cell death and differentiation 2014-07, Vol.21 (7), p.1095-1106 |
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| creator | Shin, H J Kim, H Heo, R W Kim, H J Choi, W S Kwon, H M Roh, G S |
| description | Kainic acid (KA)-induced seizures followed by neuronal death are associated with neuroinflammation and blood–brain barrier (BBB) leakage. Tonicity-responsive enhancer binding protein (TonEBP) is known as a transcriptional factor activating osmoprotective genes, and in brain, it is expressed in neuronal nuclei. Thus dysregulation of TonEBP may be involved in the pathology of KA-induced seizures. Here we used TonEBP heterozygote (+/−) mice to study the roles of TonEBP. Electroencephalographic study showed that TonEBP (+/−) mice reduced seizure frequency and severity compared with wild type during KA-induced status epilepticus. Immunohistochemistry and western blotting analysis showed that KA-induced neuroinflammation and BBB leakage were dramatically reduced in TonEBP (+/−) mice. Similarly, TonEBP-specific siRNA reduced glutamate-induced death in HT22 hippocampal neuronal cells. TonEBP haplodeficiency prevented KA-induced nuclear translocation of NF-
κ
B p65 and attenuated inflammation. Our findings identify TonEBP as a critical regulator of neuroinflammation and BBB leakage in KA-induced seizures, which suggests TonEBP as a good therapeutic target. |
| doi_str_mv | 10.1038/cdd.2014.29 |
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κ
B p65 and attenuated inflammation. Our findings identify TonEBP as a critical regulator of neuroinflammation and BBB leakage in KA-induced seizures, which suggests TonEBP as a good therapeutic target.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/cdd.2014.29</identifier><identifier>PMID: 24608792</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/250/256 ; 631/378/1934 ; 631/378/371 ; 692/699/375/178 ; Active Transport, Cell Nucleus ; Animals ; Apoptosis ; Aquaporin 4 - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Blood-Brain Barrier - metabolism ; CA3 Region, Hippocampal - immunology ; CA3 Region, Hippocampal - pathology ; Cell Biology ; Cell Cycle Analysis ; Cell Line ; Cell Nucleus - metabolism ; Cyclooxygenase 2 - metabolism ; Haploinsufficiency ; Kainic Acid ; Life Sciences ; Male ; Mice, Inbred ICR ; NF-kappa B - physiology ; Original Paper ; Seizures - chemically induced ; Seizures - immunology ; Seizures - metabolism ; Stem Cells ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Cell death and differentiation, 2014-07, Vol.21 (7), p.1095-1106</ispartof><rights>Macmillan Publishers Limited 2014</rights><rights>Copyright © 2014 Macmillan Publishers Limited 2014 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-d94ffea0918610f975c8aa59b48fcd89e446bf1cde8c89bcbd57faf5bfa6d7c03</citedby><cites>FETCH-LOGICAL-c451t-d94ffea0918610f975c8aa59b48fcd89e446bf1cde8c89bcbd57faf5bfa6d7c03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207478/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207478/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24608792$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, H J</creatorcontrib><creatorcontrib>Kim, H</creatorcontrib><creatorcontrib>Heo, R W</creatorcontrib><creatorcontrib>Kim, H J</creatorcontrib><creatorcontrib>Choi, W S</creatorcontrib><creatorcontrib>Kwon, H M</creatorcontrib><creatorcontrib>Roh, G S</creatorcontrib><title>Tonicity-responsive enhancer binding protein haplodeficiency attenuates seizure severity and NF-κB-mediated neuroinflammation in kainic acid-induced seizures</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Kainic acid (KA)-induced seizures followed by neuronal death are associated with neuroinflammation and blood–brain barrier (BBB) leakage. Tonicity-responsive enhancer binding protein (TonEBP) is known as a transcriptional factor activating osmoprotective genes, and in brain, it is expressed in neuronal nuclei. Thus dysregulation of TonEBP may be involved in the pathology of KA-induced seizures. Here we used TonEBP heterozygote (+/−) mice to study the roles of TonEBP. Electroencephalographic study showed that TonEBP (+/−) mice reduced seizure frequency and severity compared with wild type during KA-induced status epilepticus. Immunohistochemistry and western blotting analysis showed that KA-induced neuroinflammation and BBB leakage were dramatically reduced in TonEBP (+/−) mice. Similarly, TonEBP-specific siRNA reduced glutamate-induced death in HT22 hippocampal neuronal cells. TonEBP haplodeficiency prevented KA-induced nuclear translocation of NF-
κ
B p65 and attenuated inflammation. Our findings identify TonEBP as a critical regulator of neuroinflammation and BBB leakage in KA-induced seizures, which suggests TonEBP as a good therapeutic target.</description><subject>631/250/256</subject><subject>631/378/1934</subject><subject>631/378/371</subject><subject>692/699/375/178</subject><subject>Active Transport, Cell Nucleus</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Aquaporin 4 - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>CA3 Region, Hippocampal - immunology</subject><subject>CA3 Region, Hippocampal - pathology</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell Line</subject><subject>Cell Nucleus - metabolism</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Haploinsufficiency</subject><subject>Kainic Acid</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Mice, Inbred ICR</subject><subject>NF-kappa B - physiology</subject><subject>Original Paper</subject><subject>Seizures - chemically induced</subject><subject>Seizures - immunology</subject><subject>Seizures - metabolism</subject><subject>Stem Cells</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkcGKFDEQhhtR3HX15F1yFLTHpCedTi6CLq4Ki17Wc6hOKjNZu5M26R4YH8YH8SF8JjPMuCh4qkB9-aqov6qeMrpidC1fGWtXDWV81ah71TnjnahbTtf3y3vd0lpR3p1Vj3K-pZSKTomH1VnDBZWdas6rHzcxeOPnfZ0wTzFkv0OCYQvBYCK9D9aHDZlSnNEHsoVpiBZd-YHB7AnMM4YFZswko_--JCx1h6n4CARLPl3Vv36-rUe0vkCWBFxS9MENMI4w-xhIkX4FX1YgYLyty7zFFPBky4-rBw6GjE9O9aL6cvXu5vJDff35_cfLN9e14S2ba6u4cwhUMSkYdaprjQRoVc-lM1Yq5Fz0jhmL0kjVm962nQPX9g6E7QxdX1Svj95p6cu2BsOcYNBT8iOkvY7g9b-d4Ld6E3eaN7TjnSyC5ydBit8WzLMefTY4DBAwLlkz0XIhFeOHWS-OqEkx54Tubgyj-pCoLonqQ6K6UYV-9vdmd-yfCAvw8gjk0gobTPo2LimUa_3X9xveuLNx</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Shin, H J</creator><creator>Kim, H</creator><creator>Heo, R W</creator><creator>Kim, H J</creator><creator>Choi, W S</creator><creator>Kwon, H M</creator><creator>Roh, G S</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7TK</scope><scope>5PM</scope></search><sort><creationdate>20140701</creationdate><title>Tonicity-responsive enhancer binding protein haplodeficiency attenuates seizure severity and NF-κB-mediated neuroinflammation in kainic acid-induced seizures</title><author>Shin, H J ; Kim, H ; Heo, R W ; Kim, H J ; Choi, W S ; Kwon, H M ; Roh, G S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-d94ffea0918610f975c8aa59b48fcd89e446bf1cde8c89bcbd57faf5bfa6d7c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/250/256</topic><topic>631/378/1934</topic><topic>631/378/371</topic><topic>692/699/375/178</topic><topic>Active Transport, Cell Nucleus</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Aquaporin 4 - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>CA3 Region, Hippocampal - immunology</topic><topic>CA3 Region, Hippocampal - pathology</topic><topic>Cell Biology</topic><topic>Cell Cycle Analysis</topic><topic>Cell Line</topic><topic>Cell Nucleus - metabolism</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Haploinsufficiency</topic><topic>Kainic Acid</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Mice, Inbred ICR</topic><topic>NF-kappa B - physiology</topic><topic>Original Paper</topic><topic>Seizures - chemically induced</topic><topic>Seizures - immunology</topic><topic>Seizures - metabolism</topic><topic>Stem Cells</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, H J</creatorcontrib><creatorcontrib>Kim, H</creatorcontrib><creatorcontrib>Heo, R W</creatorcontrib><creatorcontrib>Kim, H J</creatorcontrib><creatorcontrib>Choi, W S</creatorcontrib><creatorcontrib>Kwon, H M</creatorcontrib><creatorcontrib>Roh, G S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, H J</au><au>Kim, H</au><au>Heo, R W</au><au>Kim, H J</au><au>Choi, W S</au><au>Kwon, H M</au><au>Roh, G S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tonicity-responsive enhancer binding protein haplodeficiency attenuates seizure severity and NF-κB-mediated neuroinflammation in kainic acid-induced seizures</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>21</volume><issue>7</issue><spage>1095</spage><epage>1106</epage><pages>1095-1106</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Kainic acid (KA)-induced seizures followed by neuronal death are associated with neuroinflammation and blood–brain barrier (BBB) leakage. Tonicity-responsive enhancer binding protein (TonEBP) is known as a transcriptional factor activating osmoprotective genes, and in brain, it is expressed in neuronal nuclei. Thus dysregulation of TonEBP may be involved in the pathology of KA-induced seizures. Here we used TonEBP heterozygote (+/−) mice to study the roles of TonEBP. Electroencephalographic study showed that TonEBP (+/−) mice reduced seizure frequency and severity compared with wild type during KA-induced status epilepticus. Immunohistochemistry and western blotting analysis showed that KA-induced neuroinflammation and BBB leakage were dramatically reduced in TonEBP (+/−) mice. Similarly, TonEBP-specific siRNA reduced glutamate-induced death in HT22 hippocampal neuronal cells. TonEBP haplodeficiency prevented KA-induced nuclear translocation of NF-
κ
B p65 and attenuated inflammation. Our findings identify TonEBP as a critical regulator of neuroinflammation and BBB leakage in KA-induced seizures, which suggests TonEBP as a good therapeutic target.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24608792</pmid><doi>10.1038/cdd.2014.29</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/250/256 631/378/1934 631/378/371 692/699/375/178 Active Transport, Cell Nucleus Animals Apoptosis Aquaporin 4 - metabolism Biochemistry Biomedical and Life Sciences Blood-Brain Barrier - metabolism CA3 Region, Hippocampal - immunology CA3 Region, Hippocampal - pathology Cell Biology Cell Cycle Analysis Cell Line Cell Nucleus - metabolism Cyclooxygenase 2 - metabolism Haploinsufficiency Kainic Acid Life Sciences Male Mice, Inbred ICR NF-kappa B - physiology Original Paper Seizures - chemically induced Seizures - immunology Seizures - metabolism Stem Cells Transcription Factors - genetics Transcription Factors - metabolism Vascular Endothelial Growth Factor A - metabolism |
| title | Tonicity-responsive enhancer binding protein haplodeficiency attenuates seizure severity and NF-κB-mediated neuroinflammation in kainic acid-induced seizures |
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