Neuronal MHC Class I Expression Is Regulated by Activity Driven Calcium Signaling
MHC class I (MHC-I) molecules are important components of the immune system. Recently MHC-I have been reported to also play important roles in brain development and synaptic plasticity. In this study, we examine the molecular mechanism(s) underlying activity-dependent MHC-I expression using hippocam...
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| Veröffentlicht in: | PloS one 2015-08, Vol.10 (8), p.e0135223-e0135223 |
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| creator | Lv, Dan Shen, Yuqing Peng, Yaqin Liu, Jiane Miao, Fengqin Zhang, Jianqiong |
| description | MHC class I (MHC-I) molecules are important components of the immune system. Recently MHC-I have been reported to also play important roles in brain development and synaptic plasticity. In this study, we examine the molecular mechanism(s) underlying activity-dependent MHC-I expression using hippocampal neurons. Here we report that neuronal expression level of MHC-I is dynamically regulated during hippocampal development after birth in vivo. Kainic acid (KA) treatment significantly increases the expression of MHC-I in cultured hippocampal neurons in vitro, suggesting that MHC-I expression is regulated by neuronal activity. In addition, KA stimulation decreased the expression of pre- and post-synaptic proteins. This down-regulation is prevented by addition of an MHC-I antibody to KA treated neurons. Further studies demonstrate that calcium-dependent protein kinase C (PKC) is important in relaying KA simulation activation signals to up-regulated MHC-I expression. This signaling cascade relies on activation of the MAPK pathway, which leads to increased phosphorylation of CREB and NF-κB p65 while also enhancing the expression of IRF-1. Together, these results suggest that expression of MHC-I in hippocampal neurons is driven by Ca2+ regulated activation of the MAPK signaling transduction cascade. |
| doi_str_mv | 10.1371/journal.pone.0135223 |
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Recently MHC-I have been reported to also play important roles in brain development and synaptic plasticity. In this study, we examine the molecular mechanism(s) underlying activity-dependent MHC-I expression using hippocampal neurons. Here we report that neuronal expression level of MHC-I is dynamically regulated during hippocampal development after birth in vivo. Kainic acid (KA) treatment significantly increases the expression of MHC-I in cultured hippocampal neurons in vitro, suggesting that MHC-I expression is regulated by neuronal activity. In addition, KA stimulation decreased the expression of pre- and post-synaptic proteins. This down-regulation is prevented by addition of an MHC-I antibody to KA treated neurons. Further studies demonstrate that calcium-dependent protein kinase C (PKC) is important in relaying KA simulation activation signals to up-regulated MHC-I expression. This signaling cascade relies on activation of the MAPK pathway, which leads to increased phosphorylation of CREB and NF-κB p65 while also enhancing the expression of IRF-1. Together, these results suggest that expression of MHC-I in hippocampal neurons is driven by Ca2+ regulated activation of the MAPK signaling transduction cascade.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0135223</identifier><identifier>PMID: 26263390</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Animals ; Brain ; Brain research ; Calcium ; Calcium ions ; Calcium Signaling ; Calcium signalling ; Cell Line ; Cellular signal transduction ; Cyclic AMP response element-binding protein ; Cyclic AMP Response Element-Binding Protein - metabolism ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Deoxyribonucleic acid ; Developmental plasticity ; DNA ; Education ; Gene expression ; Gene Expression Regulation - drug effects ; Genes, MHC Class I ; Genetic engineering ; Hippocampus ; Hippocampus - metabolism ; Immune system ; Immunology ; Interferon regulatory factor 1 ; Interferon Regulatory Factor-1 - metabolism ; Kainic acid ; Kainic Acid - pharmacology ; Kinases ; Laboratories ; Major histocompatibility complex ; MAP kinase ; MAP Kinase Signaling System - drug effects ; Medical schools ; Mice ; Molecular chains ; Nervous system ; Neurons ; Neurons - metabolism ; Neurosciences ; NF-kappa B - metabolism ; NF-κB protein ; Phosphorylation ; Protein kinase C ; Protein Kinase C - metabolism ; Proteins ; Pyramidal Cells - metabolism ; Relaying ; RNA, Messenger ; Signal transduction ; Synapses - metabolism ; Synaptic plasticity ; Synaptogenesis ; Transcription factors ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2015-08, Vol.10 (8), p.e0135223-e0135223</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Lv et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Lv et al 2015 Lv et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-778abc9482f2305cb003268fde9d43a5b43d51478a8a8ce597b0416345e652ba3</citedby><cites>FETCH-LOGICAL-c692t-778abc9482f2305cb003268fde9d43a5b43d51478a8a8ce597b0416345e652ba3</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/PMC4532511/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532511/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26263390$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yang, Yanmin</contributor><creatorcontrib>Lv, Dan</creatorcontrib><creatorcontrib>Shen, Yuqing</creatorcontrib><creatorcontrib>Peng, Yaqin</creatorcontrib><creatorcontrib>Liu, Jiane</creatorcontrib><creatorcontrib>Miao, Fengqin</creatorcontrib><creatorcontrib>Zhang, Jianqiong</creatorcontrib><title>Neuronal MHC Class I Expression Is Regulated by Activity Driven Calcium Signaling</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>MHC class I (MHC-I) molecules are important components of the immune system. Recently MHC-I have been reported to also play important roles in brain development and synaptic plasticity. In this study, we examine the molecular mechanism(s) underlying activity-dependent MHC-I expression using hippocampal neurons. Here we report that neuronal expression level of MHC-I is dynamically regulated during hippocampal development after birth in vivo. Kainic acid (KA) treatment significantly increases the expression of MHC-I in cultured hippocampal neurons in vitro, suggesting that MHC-I expression is regulated by neuronal activity. In addition, KA stimulation decreased the expression of pre- and post-synaptic proteins. This down-regulation is prevented by addition of an MHC-I antibody to KA treated neurons. Further studies demonstrate that calcium-dependent protein kinase C (PKC) is important in relaying KA simulation activation signals to up-regulated MHC-I expression. This signaling cascade relies on activation of the MAPK pathway, which leads to increased phosphorylation of CREB and NF-κB p65 while also enhancing the expression of IRF-1. Together, these results suggest that expression of MHC-I in hippocampal neurons is driven by Ca2+ regulated activation of the MAPK signaling transduction cascade.</description><subject>Activation</subject><subject>Animals</subject><subject>Brain</subject><subject>Brain research</subject><subject>Calcium</subject><subject>Calcium ions</subject><subject>Calcium Signaling</subject><subject>Calcium signalling</subject><subject>Cell Line</subject><subject>Cellular signal transduction</subject><subject>Cyclic AMP response element-binding protein</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>Developmental plasticity</subject><subject>DNA</subject><subject>Education</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes, MHC Class I</subject><subject>Genetic engineering</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Interferon regulatory factor 1</subject><subject>Interferon Regulatory Factor-1 - metabolism</subject><subject>Kainic acid</subject><subject>Kainic Acid - pharmacology</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Major histocompatibility complex</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Medical schools</subject><subject>Mice</subject><subject>Molecular chains</subject><subject>Nervous system</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Phosphorylation</subject><subject>Protein kinase C</subject><subject>Protein Kinase C - metabolism</subject><subject>Proteins</subject><subject>Pyramidal Cells - metabolism</subject><subject>Relaying</subject><subject>RNA, Messenger</subject><subject>Signal transduction</subject><subject>Synapses - metabolism</subject><subject>Synaptic plasticity</subject><subject>Synaptogenesis</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor-TNF</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1v0zAUhiMEYqPwDxBYQkJw0eLPfNxMqspglQYTG3Br2Y6TunLjYifV-u9x1mxq0C7QkWzLfs5r-5w3SV4jOEMkQ5_WrvONsLOta_QMIsIwJk-SU1QQPE0xJE-P1ifJixDWEDKSp-nz5ASnOCWkgKfJj--68y7qgG8XC7CwIgSwBOe3W69DMK4BywCudd1Z0eoSyD2Yq9bsTLsHn73Z6QYshFWm24AbU0cV09Qvk2eVsEG_GuZJ8uvL-c_FxfTy6utyMb-cqrTA7TTLciFVQXNcYQKZkhASnOZVqYuSEsEkJSVDNFIxlGZFJiFFKaFMpwxLQSbJ24Pu1rrAh2oEjjKYM5znFEZieSBKJ9Z8681G-D13wvC7DedrLnxrlNUcEZlnDPVvqahQuJCSkEpJlWORYYqi1tlwWyc3ulS6ab2wI9HxSWNWvHY7ThnBDPUCHwYB7_50OrR8Y4LS1opGu-7u3bGrRZ716Lt_0Md_N1C1iB8wTeXivaoX5XOKGUGoHyfJ7BEqRqk3RkXrVCbujxI-jhIi0-rbthZdCHx5c_3_7NXvMfv-iF1pYdtVcLZro8nCGKQHUHkXgtfVQ5ER5L3z76vBe-fzwfkx7c1xgx6S7q1O_gJ1i_so</recordid><startdate>20150811</startdate><enddate>20150811</enddate><creator>Lv, Dan</creator><creator>Shen, Yuqing</creator><creator>Peng, Yaqin</creator><creator>Liu, Jiane</creator><creator>Miao, Fengqin</creator><creator>Zhang, Jianqiong</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150811</creationdate><title>Neuronal MHC Class I Expression Is Regulated by Activity Driven Calcium Signaling</title><author>Lv, Dan ; Shen, Yuqing ; Peng, Yaqin ; Liu, Jiane ; Miao, Fengqin ; Zhang, Jianqiong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-778abc9482f2305cb003268fde9d43a5b43d51478a8a8ce597b0416345e652ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Activation</topic><topic>Animals</topic><topic>Brain</topic><topic>Brain research</topic><topic>Calcium</topic><topic>Calcium ions</topic><topic>Calcium Signaling</topic><topic>Calcium signalling</topic><topic>Cell Line</topic><topic>Cellular signal transduction</topic><topic>Cyclic AMP response element-binding protein</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>Developmental plasticity</topic><topic>DNA</topic><topic>Education</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes, MHC Class I</topic><topic>Genetic engineering</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Interferon regulatory factor 1</topic><topic>Interferon Regulatory Factor-1 - metabolism</topic><topic>Kainic acid</topic><topic>Kainic Acid - pharmacology</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Major histocompatibility complex</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Medical schools</topic><topic>Mice</topic><topic>Molecular chains</topic><topic>Nervous system</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>NF-kappa B - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lv, Dan</au><au>Shen, Yuqing</au><au>Peng, Yaqin</au><au>Liu, Jiane</au><au>Miao, Fengqin</au><au>Zhang, Jianqiong</au><au>Yang, Yanmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuronal MHC Class I Expression Is Regulated by Activity Driven Calcium Signaling</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-08-11</date><risdate>2015</risdate><volume>10</volume><issue>8</issue><spage>e0135223</spage><epage>e0135223</epage><pages>e0135223-e0135223</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>MHC class I (MHC-I) molecules are important components of the immune system. Recently MHC-I have been reported to also play important roles in brain development and synaptic plasticity. In this study, we examine the molecular mechanism(s) underlying activity-dependent MHC-I expression using hippocampal neurons. Here we report that neuronal expression level of MHC-I is dynamically regulated during hippocampal development after birth in vivo. Kainic acid (KA) treatment significantly increases the expression of MHC-I in cultured hippocampal neurons in vitro, suggesting that MHC-I expression is regulated by neuronal activity. In addition, KA stimulation decreased the expression of pre- and post-synaptic proteins. This down-regulation is prevented by addition of an MHC-I antibody to KA treated neurons. Further studies demonstrate that calcium-dependent protein kinase C (PKC) is important in relaying KA simulation activation signals to up-regulated MHC-I expression. This signaling cascade relies on activation of the MAPK pathway, which leads to increased phosphorylation of CREB and NF-κB p65 while also enhancing the expression of IRF-1. Together, these results suggest that expression of MHC-I in hippocampal neurons is driven by Ca2+ regulated activation of the MAPK signaling transduction cascade.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26263390</pmid><doi>10.1371/journal.pone.0135223</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Activation Animals Brain Brain research Calcium Calcium ions Calcium Signaling Calcium signalling Cell Line Cellular signal transduction Cyclic AMP response element-binding protein Cyclic AMP Response Element-Binding Protein - metabolism Cyclic AMP-Dependent Protein Kinases - metabolism Deoxyribonucleic acid Developmental plasticity DNA Education Gene expression Gene Expression Regulation - drug effects Genes, MHC Class I Genetic engineering Hippocampus Hippocampus - metabolism Immune system Immunology Interferon regulatory factor 1 Interferon Regulatory Factor-1 - metabolism Kainic acid Kainic Acid - pharmacology Kinases Laboratories Major histocompatibility complex MAP kinase MAP Kinase Signaling System - drug effects Medical schools Mice Molecular chains Nervous system Neurons Neurons - metabolism Neurosciences NF-kappa B - metabolism NF-κB protein Phosphorylation Protein kinase C Protein Kinase C - metabolism Proteins Pyramidal Cells - metabolism Relaying RNA, Messenger Signal transduction Synapses - metabolism Synaptic plasticity Synaptogenesis Transcription factors Tumor necrosis factor-TNF |
| title | Neuronal MHC Class I Expression Is Regulated by Activity Driven Calcium Signaling |
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