Opposite effects of HDAC5 and p300 on MRTF-A-related neuronal apoptosis during ischemia/reperfusion injury in rats
Our recent study has revealed that the myocardin-related transcription factor-A (MRTF-A) is involved in the apoptosis of cortical neurons induced by ischemia/reperfusion (I/R). Histone deacetylase 5 (HDAC5) and histone acetyltransferase p300 (P300) are two well-known regulators for transcription fac...
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| creator | Li, Na Yuan, Qiong Cao, Xiao-Lu Zhang, Ying Min, Zhen-Li Xu, Shi-Qiang Yu, Zhi-Jun Cheng, Jing Zhang, Chunxiang Hu, Xia-Min |
| description | Our recent study has revealed that the myocardin-related transcription factor-A (MRTF-A) is involved in the apoptosis of cortical neurons induced by ischemia/reperfusion (I/R). Histone deacetylase 5 (HDAC5) and histone acetyltransferase p300 (P300) are two well-known regulators for transcription factors; however, their roles in MRTF-A-related effect on neuronal injuries during I/R are still unclear. In this study, in a model rat cerebral I/R injury via middle cerebral artery occlusion and reperfusion, we found that the expression and activity of HDAC5 was upregulated, whereas p300 and MRTF-A were downregulated both in expression and activity during I/R. Their expression changes and the interaction of the MRTF-A with HDAC5 or p300 were further verified by double immunofluorescence and co-immunoprecipitation. In cultured neuronal apoptosis model induced by H
2
O
2
, MRTF-A exhibited an anti-apoptotic effect by enhancing the transcription of Bcl-2 and Mcl-1 via CArG box binding. MRTF-A-induced anti-apoptotic effect was effectively inhibited by HDAC5, but was significantly enhanced by p300. The results suggest that both HDAC5 and p300 are involved in MRTF-A-mediated effect on neuronal apoptosis during ischemia/reperfusion injury, but with opposite effects. |
| doi_str_mv | 10.1038/cddis.2017.16 |
| format | Article |
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2
O
2
, MRTF-A exhibited an anti-apoptotic effect by enhancing the transcription of Bcl-2 and Mcl-1 via CArG box binding. MRTF-A-induced anti-apoptotic effect was effectively inhibited by HDAC5, but was significantly enhanced by p300. The results suggest that both HDAC5 and p300 are involved in MRTF-A-mediated effect on neuronal apoptosis during ischemia/reperfusion injury, but with opposite effects.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/cddis.2017.16</identifier><identifier>PMID: 28230854</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/2 ; 13/31 ; 631/443/592/75/593/1370 ; 631/443/592/75/593/15/1939 ; 631/80/82/23 ; 631/80/86 ; 96 ; 96/2 ; Animals ; Antibodies ; Apoptosis - physiology ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; E1A-Associated p300 Protein - metabolism ; Histone Deacetylases - metabolism ; Immunology ; Life Sciences ; Male ; Myeloid Cell Leukemia Sequence 1 Protein - metabolism ; Neurons - metabolism ; Original ; original-article ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Transcription Factors - metabolism ; Transcription, Genetic - physiology</subject><ispartof>Cell death & disease, 2017-02, Vol.8 (2), p.e2624-e2624</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Feb 2017</rights><rights>Copyright © 2017 The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c384t-3c852278eec25f8ed180ae917612f839a8435bad6a57f19e6e1bf3a9dff8808b3</citedby><cites>FETCH-LOGICAL-c384t-3c852278eec25f8ed180ae917612f839a8435bad6a57f19e6e1bf3a9dff8808b3</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/PMC5386465/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386465/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28230854$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Yuan, Qiong</creatorcontrib><creatorcontrib>Cao, Xiao-Lu</creatorcontrib><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Min, Zhen-Li</creatorcontrib><creatorcontrib>Xu, Shi-Qiang</creatorcontrib><creatorcontrib>Yu, Zhi-Jun</creatorcontrib><creatorcontrib>Cheng, Jing</creatorcontrib><creatorcontrib>Zhang, Chunxiang</creatorcontrib><creatorcontrib>Hu, Xia-Min</creatorcontrib><title>Opposite effects of HDAC5 and p300 on MRTF-A-related neuronal apoptosis during ischemia/reperfusion injury in rats</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Our recent study has revealed that the myocardin-related transcription factor-A (MRTF-A) is involved in the apoptosis of cortical neurons induced by ischemia/reperfusion (I/R). Histone deacetylase 5 (HDAC5) and histone acetyltransferase p300 (P300) are two well-known regulators for transcription factors; however, their roles in MRTF-A-related effect on neuronal injuries during I/R are still unclear. In this study, in a model rat cerebral I/R injury via middle cerebral artery occlusion and reperfusion, we found that the expression and activity of HDAC5 was upregulated, whereas p300 and MRTF-A were downregulated both in expression and activity during I/R. Their expression changes and the interaction of the MRTF-A with HDAC5 or p300 were further verified by double immunofluorescence and co-immunoprecipitation. In cultured neuronal apoptosis model induced by H
2
O
2
, MRTF-A exhibited an anti-apoptotic effect by enhancing the transcription of Bcl-2 and Mcl-1 via CArG box binding. MRTF-A-induced anti-apoptotic effect was effectively inhibited by HDAC5, but was significantly enhanced by p300. The results suggest that both HDAC5 and p300 are involved in MRTF-A-mediated effect on neuronal apoptosis during ischemia/reperfusion injury, but with opposite effects.</description><subject>13</subject><subject>13/2</subject><subject>13/31</subject><subject>631/443/592/75/593/1370</subject><subject>631/443/592/75/593/15/1939</subject><subject>631/80/82/23</subject><subject>631/80/86</subject><subject>96</subject><subject>96/2</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis - physiology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>E1A-Associated p300 Protein - metabolism</subject><subject>Histone Deacetylases - metabolism</subject><subject>Immunology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Myeloid Cell Leukemia Sequence 1 Protein - metabolism</subject><subject>Neurons - metabolism</subject><subject>Original</subject><subject>original-article</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic - physiology</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkd9rFDEQx4MottQ--ioBX3zZa35sdmdfhOO0VqgUpD6H3GbS5thL1mS30P_erFfLKc7LDOQz38nMl5C3nK04k3DRW-vzSjDernjzgpwKVvOqBuheHtUn5DznHSshJROqeU1OBAjJQNWnJN2MY8x-QorOYT9lGh29-rTeKGqCpaNkjMZAv32_vazWVcLBTGhpwDnFYAZqxjhOpT9TOycf7qjP_T3uvblIOGJyc_al24fdnB5LoslM-Q155cyQ8fwpn5Efl59vN1fV9c2Xr5v1ddVLqKdK9qCEaAGxF8oBWg7MYMfbhgsHsjNQS7U1tjGqdbzDBvnWSdNZ5wAYbOUZ-XjQHeftHm2PYUpm0GPye5MedTRe__0S_L2-iw9aSWjqRhWBD08CKf6cMU96X9bDYTAB45w1h5YrxVi9oO__QXdxTuVCC9XxggGvC1UdqD7FnBO6589wphdD9W9D9WKo5k3h3x1v8Ez_sa8AqwOQx-X6mI7G_lfxFy_trIE</recordid><startdate>20170223</startdate><enddate>20170223</enddate><creator>Li, Na</creator><creator>Yuan, Qiong</creator><creator>Cao, Xiao-Lu</creator><creator>Zhang, Ying</creator><creator>Min, Zhen-Li</creator><creator>Xu, Shi-Qiang</creator><creator>Yu, Zhi-Jun</creator><creator>Cheng, Jing</creator><creator>Zhang, Chunxiang</creator><creator>Hu, Xia-Min</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><general>Nature Publishing Group</general><scope>C6C</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170223</creationdate><title>Opposite effects of HDAC5 and p300 on MRTF-A-related neuronal apoptosis during ischemia/reperfusion injury in rats</title><author>Li, Na ; Yuan, Qiong ; Cao, Xiao-Lu ; Zhang, Ying ; Min, Zhen-Li ; Xu, Shi-Qiang ; Yu, Zhi-Jun ; Cheng, Jing ; Zhang, Chunxiang ; Hu, Xia-Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c384t-3c852278eec25f8ed180ae917612f839a8435bad6a57f19e6e1bf3a9dff8808b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13</topic><topic>13/2</topic><topic>13/31</topic><topic>631/443/592/75/593/1370</topic><topic>631/443/592/75/593/15/1939</topic><topic>631/80/82/23</topic><topic>631/80/86</topic><topic>96</topic><topic>96/2</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis - physiology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>E1A-Associated p300 Protein - metabolism</topic><topic>Histone Deacetylases - metabolism</topic><topic>Immunology</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Myeloid Cell Leukemia Sequence 1 Protein - metabolism</topic><topic>Neurons - metabolism</topic><topic>Original</topic><topic>original-article</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription, Genetic - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Yuan, Qiong</creatorcontrib><creatorcontrib>Cao, Xiao-Lu</creatorcontrib><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Min, Zhen-Li</creatorcontrib><creatorcontrib>Xu, Shi-Qiang</creatorcontrib><creatorcontrib>Yu, Zhi-Jun</creatorcontrib><creatorcontrib>Cheng, Jing</creatorcontrib><creatorcontrib>Zhang, Chunxiang</creatorcontrib><creatorcontrib>Hu, Xia-Min</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Na</au><au>Yuan, Qiong</au><au>Cao, Xiao-Lu</au><au>Zhang, Ying</au><au>Min, Zhen-Li</au><au>Xu, Shi-Qiang</au><au>Yu, Zhi-Jun</au><au>Cheng, Jing</au><au>Zhang, Chunxiang</au><au>Hu, Xia-Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Opposite effects of HDAC5 and p300 on MRTF-A-related neuronal apoptosis during ischemia/reperfusion injury in rats</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2017-02-23</date><risdate>2017</risdate><volume>8</volume><issue>2</issue><spage>e2624</spage><epage>e2624</epage><pages>e2624-e2624</pages><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Our recent study has revealed that the myocardin-related transcription factor-A (MRTF-A) is involved in the apoptosis of cortical neurons induced by ischemia/reperfusion (I/R). Histone deacetylase 5 (HDAC5) and histone acetyltransferase p300 (P300) are two well-known regulators for transcription factors; however, their roles in MRTF-A-related effect on neuronal injuries during I/R are still unclear. In this study, in a model rat cerebral I/R injury via middle cerebral artery occlusion and reperfusion, we found that the expression and activity of HDAC5 was upregulated, whereas p300 and MRTF-A were downregulated both in expression and activity during I/R. Their expression changes and the interaction of the MRTF-A with HDAC5 or p300 were further verified by double immunofluorescence and co-immunoprecipitation. In cultured neuronal apoptosis model induced by H
2
O
2
, MRTF-A exhibited an anti-apoptotic effect by enhancing the transcription of Bcl-2 and Mcl-1 via CArG box binding. MRTF-A-induced anti-apoptotic effect was effectively inhibited by HDAC5, but was significantly enhanced by p300. The results suggest that both HDAC5 and p300 are involved in MRTF-A-mediated effect on neuronal apoptosis during ischemia/reperfusion injury, but with opposite effects.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28230854</pmid><doi>10.1038/cddis.2017.16</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/2 13/31 631/443/592/75/593/1370 631/443/592/75/593/15/1939 631/80/82/23 631/80/86 96 96/2 Animals Antibodies Apoptosis - physiology Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture E1A-Associated p300 Protein - metabolism Histone Deacetylases - metabolism Immunology Life Sciences Male Myeloid Cell Leukemia Sequence 1 Protein - metabolism Neurons - metabolism Original original-article Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Rats, Sprague-Dawley Reperfusion Injury - metabolism Reperfusion Injury - pathology Transcription Factors - metabolism Transcription, Genetic - physiology |
| title | Opposite effects of HDAC5 and p300 on MRTF-A-related neuronal apoptosis during ischemia/reperfusion injury in rats |
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