Inhibition of histone H3K9 acetylation by anacardic acid can correct the over-expression of Gata4 in the hearts of fetal mice exposed to alcohol during pregnancy
Cardiovascular malformations can be caused by abnormalities in Gata4 expression during fetal development. In a previous study, we demonstrated that ethanol exposure could lead to histone hyperacetylation and Gata4 over-expression in fetal mouse hearts. However, the potential mechanisms of histone hy...
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| description | Cardiovascular malformations can be caused by abnormalities in Gata4 expression during fetal development. In a previous study, we demonstrated that ethanol exposure could lead to histone hyperacetylation and Gata4 over-expression in fetal mouse hearts. However, the potential mechanisms of histone hyperacetylation and Gata4 over-expression induced by ethanol remain unclear.
Pregnant mice were gavaged with ethanol or saline. Fetal mouse hearts were collected for analysis. The results of ethanol fed groups showed that global HAT activity was unusually high in the hearts of fetal mice while global HDAC activity remained unchanged. Binding of P300, CBP, PCAF, SRC1, but not GCN5, were increased on the Gata4 promoter relative to the saline treated group. Increased acetylation of H3K9 and increased mRNA expression of Gata4, α-MHC, cTnT were observed in these hearts. Treatment with the pan-histone acetylase inhibitor, anacardic acid, reduced the binding of P300, PCAF to the Gata4 promoter and reversed H3K9 hyperacetylation in the presence of ethanol. Interestingly, anacardic acid attenuated over-expression of Gata4, α-MHC and cTnT in fetal mouse hearts exposed to ethanol.
Our results suggest that P300 and PCAF may be critical regulatory factors that mediate Gata4 over-expression induced by ethanol exposure. Alternatively, P300, PCAF and Gata4 may coordinate over-expression of cardiac downstream genes in mouse hearts exposed to ethanol. Anacardic acid may thus protect against ethanol-induced Gata4, α-MHC, cTnT over-expression by inhibiting the binding of P300 and PCAF to the promoter region of these genes. |
| doi_str_mv | 10.1371/journal.pone.0104135 |
| format | Article |
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Pregnant mice were gavaged with ethanol or saline. Fetal mouse hearts were collected for analysis. The results of ethanol fed groups showed that global HAT activity was unusually high in the hearts of fetal mice while global HDAC activity remained unchanged. Binding of P300, CBP, PCAF, SRC1, but not GCN5, were increased on the Gata4 promoter relative to the saline treated group. Increased acetylation of H3K9 and increased mRNA expression of Gata4, α-MHC, cTnT were observed in these hearts. Treatment with the pan-histone acetylase inhibitor, anacardic acid, reduced the binding of P300, PCAF to the Gata4 promoter and reversed H3K9 hyperacetylation in the presence of ethanol. Interestingly, anacardic acid attenuated over-expression of Gata4, α-MHC and cTnT in fetal mouse hearts exposed to ethanol.
Our results suggest that P300 and PCAF may be critical regulatory factors that mediate Gata4 over-expression induced by ethanol exposure. Alternatively, P300, PCAF and Gata4 may coordinate over-expression of cardiac downstream genes in mouse hearts exposed to ethanol. Anacardic acid may thus protect against ethanol-induced Gata4, α-MHC, cTnT over-expression by inhibiting the binding of P300 and PCAF to the promoter region of these genes.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0104135</identifier><identifier>PMID: 25101666</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; Acetates ; Acetylation ; Acetylation - drug effects ; Acids ; Alcohol ; Alcohols ; Anacardic Acids - pharmacology ; Analysis ; Animals ; Base Sequence ; Binding ; Biology and Life Sciences ; Cardiomyocytes ; Cardiovascular disease ; Child development ; Children & youth ; Chromatin ; Congenital diseases ; Cooperation ; Deoxyribonucleic acid ; DNA ; DNA methylation ; Epigenetics ; Ethanol ; Ethanol - toxicity ; Event-related potentials ; Exposure ; Female ; Fetal development ; Fetal Development - drug effects ; GATA4 Transcription Factor - chemistry ; GATA4 Transcription Factor - metabolism ; Gene expression ; Gene Expression Regulation, Developmental ; Genes ; Heart ; Heart - embryology ; Heart diseases ; Histone deacetylase ; Histones - metabolism ; Homogenization ; Hospitals ; Laboratories ; Major histocompatibility complex ; Medical research ; Medicine and Health Sciences ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Overexpression ; Pediatrics ; Pregnancy ; Pregnant women ; Prenatal Exposure Delayed Effects ; Promoter Regions, Genetic ; Proteins ; RNA ; RNA polymerase ; Sequence Analysis, DNA ; Stem cells ; Transcription factors</subject><ispartof>PloS one, 2014-08, Vol.9 (8), p.e104135</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Peng 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>2014 Peng et al 2014 Peng et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-64cedb8f24b836c032d73f30563ff3f10d8d15da783cbac136d3b88bc3babf623</citedby><cites>FETCH-LOGICAL-c758t-64cedb8f24b836c032d73f30563ff3f10d8d15da783cbac136d3b88bc3babf623</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/PMC4125174/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4125174/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25101666$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Dettman, Robert</contributor><creatorcontrib>Peng, Chang</creatorcontrib><creatorcontrib>Zhu, Jing</creatorcontrib><creatorcontrib>Sun, Hui-Chao</creatorcontrib><creatorcontrib>Huang, Xu-Pei</creatorcontrib><creatorcontrib>Zhao, Wei-An</creatorcontrib><creatorcontrib>Zheng, Min</creatorcontrib><creatorcontrib>Liu, Ling-Juan</creatorcontrib><creatorcontrib>Tian, Jie</creatorcontrib><title>Inhibition of histone H3K9 acetylation by anacardic acid can correct the over-expression of Gata4 in the hearts of fetal mice exposed to alcohol during pregnancy</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cardiovascular malformations can be caused by abnormalities in Gata4 expression during fetal development. In a previous study, we demonstrated that ethanol exposure could lead to histone hyperacetylation and Gata4 over-expression in fetal mouse hearts. However, the potential mechanisms of histone hyperacetylation and Gata4 over-expression induced by ethanol remain unclear.
Pregnant mice were gavaged with ethanol or saline. Fetal mouse hearts were collected for analysis. The results of ethanol fed groups showed that global HAT activity was unusually high in the hearts of fetal mice while global HDAC activity remained unchanged. Binding of P300, CBP, PCAF, SRC1, but not GCN5, were increased on the Gata4 promoter relative to the saline treated group. Increased acetylation of H3K9 and increased mRNA expression of Gata4, α-MHC, cTnT were observed in these hearts. Treatment with the pan-histone acetylase inhibitor, anacardic acid, reduced the binding of P300, PCAF to the Gata4 promoter and reversed H3K9 hyperacetylation in the presence of ethanol. Interestingly, anacardic acid attenuated over-expression of Gata4, α-MHC and cTnT in fetal mouse hearts exposed to ethanol.
Our results suggest that P300 and PCAF may be critical regulatory factors that mediate Gata4 over-expression induced by ethanol exposure. Alternatively, P300, PCAF and Gata4 may coordinate over-expression of cardiac downstream genes in mouse hearts exposed to ethanol. Anacardic acid may thus protect against ethanol-induced Gata4, α-MHC, cTnT over-expression by inhibiting the binding of P300 and PCAF to the promoter region of these genes.</description><subject>Abnormalities</subject><subject>Acetates</subject><subject>Acetylation</subject><subject>Acetylation - drug effects</subject><subject>Acids</subject><subject>Alcohol</subject><subject>Alcohols</subject><subject>Anacardic Acids - pharmacology</subject><subject>Analysis</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Binding</subject><subject>Biology and Life Sciences</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Child development</subject><subject>Children & youth</subject><subject>Chromatin</subject><subject>Congenital diseases</subject><subject>Cooperation</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Epigenetics</subject><subject>Ethanol</subject><subject>Ethanol - toxicity</subject><subject>Event-related potentials</subject><subject>Exposure</subject><subject>Female</subject><subject>Fetal development</subject><subject>Fetal Development - drug effects</subject><subject>GATA4 Transcription Factor - chemistry</subject><subject>GATA4 Transcription Factor - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Genes</subject><subject>Heart</subject><subject>Heart - embryology</subject><subject>Heart diseases</subject><subject>Histone deacetylase</subject><subject>Histones - metabolism</subject><subject>Homogenization</subject><subject>Hospitals</subject><subject>Laboratories</subject><subject>Major histocompatibility complex</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Molecular Sequence Data</subject><subject>Overexpression</subject><subject>Pediatrics</subject><subject>Pregnancy</subject><subject>Pregnant women</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>RNA</subject><subject>RNA polymerase</subject><subject>Sequence Analysis, DNA</subject><subject>Stem cells</subject><subject>Transcription 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of histone H3K9 acetylation by anacardic acid can correct the over-expression of Gata4 in the hearts of fetal mice exposed to alcohol during pregnancy</title><author>Peng, Chang ; Zhu, Jing ; Sun, Hui-Chao ; Huang, Xu-Pei ; Zhao, Wei-An ; Zheng, Min ; Liu, Ling-Juan ; Tian, Jie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-64cedb8f24b836c032d73f30563ff3f10d8d15da783cbac136d3b88bc3babf623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Abnormalities</topic><topic>Acetates</topic><topic>Acetylation</topic><topic>Acetylation - drug effects</topic><topic>Acids</topic><topic>Alcohol</topic><topic>Alcohols</topic><topic>Anacardic Acids - pharmacology</topic><topic>Analysis</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Binding</topic><topic>Biology and Life Sciences</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Child 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pregnancy</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-08-07</date><risdate>2014</risdate><volume>9</volume><issue>8</issue><spage>e104135</spage><pages>e104135-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cardiovascular malformations can be caused by abnormalities in Gata4 expression during fetal development. In a previous study, we demonstrated that ethanol exposure could lead to histone hyperacetylation and Gata4 over-expression in fetal mouse hearts. However, the potential mechanisms of histone hyperacetylation and Gata4 over-expression induced by ethanol remain unclear.
Pregnant mice were gavaged with ethanol or saline. Fetal mouse hearts were collected for analysis. The results of ethanol fed groups showed that global HAT activity was unusually high in the hearts of fetal mice while global HDAC activity remained unchanged. Binding of P300, CBP, PCAF, SRC1, but not GCN5, were increased on the Gata4 promoter relative to the saline treated group. Increased acetylation of H3K9 and increased mRNA expression of Gata4, α-MHC, cTnT were observed in these hearts. Treatment with the pan-histone acetylase inhibitor, anacardic acid, reduced the binding of P300, PCAF to the Gata4 promoter and reversed H3K9 hyperacetylation in the presence of ethanol. Interestingly, anacardic acid attenuated over-expression of Gata4, α-MHC and cTnT in fetal mouse hearts exposed to ethanol.
Our results suggest that P300 and PCAF may be critical regulatory factors that mediate Gata4 over-expression induced by ethanol exposure. Alternatively, P300, PCAF and Gata4 may coordinate over-expression of cardiac downstream genes in mouse hearts exposed to ethanol. Anacardic acid may thus protect against ethanol-induced Gata4, α-MHC, cTnT over-expression by inhibiting the binding of P300 and PCAF to the promoter region of these genes.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25101666</pmid><doi>10.1371/journal.pone.0104135</doi><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_plos_journals_2014047324 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Abnormalities Acetates Acetylation Acetylation - drug effects Acids Alcohol Alcohols Anacardic Acids - pharmacology Analysis Animals Base Sequence Binding Biology and Life Sciences Cardiomyocytes Cardiovascular disease Child development Children & youth Chromatin Congenital diseases Cooperation Deoxyribonucleic acid DNA DNA methylation Epigenetics Ethanol Ethanol - toxicity Event-related potentials Exposure Female Fetal development Fetal Development - drug effects GATA4 Transcription Factor - chemistry GATA4 Transcription Factor - metabolism Gene expression Gene Expression Regulation, Developmental Genes Heart Heart - embryology Heart diseases Histone deacetylase Histones - metabolism Homogenization Hospitals Laboratories Major histocompatibility complex Medical research Medicine and Health Sciences Mice Mice, Inbred Strains Molecular Sequence Data Overexpression Pediatrics Pregnancy Pregnant women Prenatal Exposure Delayed Effects Promoter Regions, Genetic Proteins RNA RNA polymerase Sequence Analysis, DNA Stem cells Transcription factors |
| title | Inhibition of histone H3K9 acetylation by anacardic acid can correct the over-expression of Gata4 in the hearts of fetal mice exposed to alcohol during pregnancy |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T02%3A27%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inhibition%20of%20histone%20H3K9%20acetylation%20by%20anacardic%20acid%20can%20correct%20the%20over-expression%20of%20Gata4%20in%20the%20hearts%20of%20fetal%20mice%20exposed%20to%20alcohol%20during%20pregnancy&rft.jtitle=PloS%20one&rft.au=Peng,%20Chang&rft.date=2014-08-07&rft.volume=9&rft.issue=8&rft.spage=e104135&rft.pages=e104135-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0104135&rft_dat=%3Cgale_plos_%3EA418708542%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2014047324&rft_id=info:pmid/25101666&rft_galeid=A418708542&rft_doaj_id=oai_doaj_org_article_9e0886ed4ba64ff9824f2f2bd7fba2cf&rfr_iscdi=true |