Fetal alcohol exposure alters proopiomelanocortin gene expression and hypothalamic-pituitary-adrenal axis function via increasing MeCP2 expression in the hypothalamus
Proopiomelanocortin (POMC) is a precursor gene of the neuropeptide β-endorphin in the hypothalamus and is known to regulate various physiological functions including stress response. Several recent reports showed that fetal alcohol exposure programs the hypothalamus to produce lower levels of POMC g...
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description | Proopiomelanocortin (POMC) is a precursor gene of the neuropeptide β-endorphin in the hypothalamus and is known to regulate various physiological functions including stress response. Several recent reports showed that fetal alcohol exposure programs the hypothalamus to produce lower levels of POMC gene transcripts and to elevate the hypothalamic-pituitary-adrenal (HPA) axis response to stressful stimuli. We investigated the role of methyl CpG binding protein (MeCP2) in the effects of prenatal ethanol on POMC gene expression and hypothalamic-pituitary-adrenal (HPA) axis function. Pregnant Sprague Dawley rats were fed between GD 7 and 21 with a liquid diet containing 6.7% alcohol, pair-fed with isocaloric liquid diet, or fed ad libitum with rat chow, and their male offsprings were used at 60 days after birth in this study. Fetal alcohol exposure reduced the level of POMC mRNA, but increased the level of DNA methylation of this gene in the arcuate nucleus (ARC) of the hypothalamus where the POMC neuronal cell bodies are located. Fetal alcohol exposed rats showed a significant increase in MeCP2 protein levels in POMC cells, MeCP2 gene transcript levels as well as increased MeCP2 protein binding on the POMC promoter in the arcuate nucleus. Lentiviral delivery of MeCP2 shRNA into the third ventricle efficiently reduced MeCP2 expression and prevented the effect of prenatal ethanol on POMC gene expression in the arcuate nucleus. MeCP2-shRNA treatment also normalized the prenatal ethanol-induced increase in corticotropin releasing hormone (CRH) gene expression in the hypothalamus and elevated plasma adrenocorticotrophic hormone (ACTH) and corticosterone hormone responses to lipopolysaccharide (LPS) challenge. These results suggest that fetal alcohol programming of POMC gene may involve recruitment of MeCP2 on to the methylated promoter of the POMC gene to suppress POMC transcript levels and contribute to HPA axis dysregulation. |
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Several recent reports showed that fetal alcohol exposure programs the hypothalamus to produce lower levels of POMC gene transcripts and to elevate the hypothalamic-pituitary-adrenal (HPA) axis response to stressful stimuli. We investigated the role of methyl CpG binding protein (MeCP2) in the effects of prenatal ethanol on POMC gene expression and hypothalamic-pituitary-adrenal (HPA) axis function. Pregnant Sprague Dawley rats were fed between GD 7 and 21 with a liquid diet containing 6.7% alcohol, pair-fed with isocaloric liquid diet, or fed ad libitum with rat chow, and their male offsprings were used at 60 days after birth in this study. Fetal alcohol exposure reduced the level of POMC mRNA, but increased the level of DNA methylation of this gene in the arcuate nucleus (ARC) of the hypothalamus where the POMC neuronal cell bodies are located. Fetal alcohol exposed rats showed a significant increase in MeCP2 protein levels in POMC cells, MeCP2 gene transcript levels as well as increased MeCP2 protein binding on the POMC promoter in the arcuate nucleus. Lentiviral delivery of MeCP2 shRNA into the third ventricle efficiently reduced MeCP2 expression and prevented the effect of prenatal ethanol on POMC gene expression in the arcuate nucleus. MeCP2-shRNA treatment also normalized the prenatal ethanol-induced increase in corticotropin releasing hormone (CRH) gene expression in the hypothalamus and elevated plasma adrenocorticotrophic hormone (ACTH) and corticosterone hormone responses to lipopolysaccharide (LPS) challenge. These results suggest that fetal alcohol programming of POMC gene may involve recruitment of MeCP2 on to the methylated promoter of the POMC gene to suppress POMC transcript levels and contribute to HPA axis dysregulation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0113228</identifier><identifier>PMID: 25409090</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adrenocorticotropic hormone ; Alcohol use ; Alcoholic beverages ; Animals ; Arcuate nucleus ; Arcuate Nucleus of Hypothalamus - metabolism ; Biology and Life Sciences ; Corticosterone ; Corticotropin-releasing hormone ; CpG islands ; Deoxyribonucleic acid ; DNA ; DNA Methylation ; Epigenetics ; Ethanol ; Ethanol - adverse effects ; Exposure ; Female ; Gene expression ; Gene Expression Regulation ; Hypothalamic-pituitary-adrenal axis ; Hypothalamo-Hypophyseal System - metabolism ; Hypothalamus ; Lipopolysaccharides ; Male ; MeCP2 protein ; Methyl-CpG binding protein ; Methyl-CpG-Binding Protein 2 - metabolism ; Nuclei (cytology) ; Pituitary ; Pituitary-Adrenal System - metabolism ; Plasmids ; Pregnancy ; Prenatal Exposure Delayed Effects - chemically induced ; Prenatal Exposure Delayed Effects - genetics ; Prenatal Exposure Delayed Effects - metabolism ; Pro-Opiomelanocortin - genetics ; Pro-Opiomelanocortin - metabolism ; Promoter Regions, Genetic ; Proopiomelanocortin ; Rats ; Rats, Sprague-Dawley ; Rodents ; Transcription ; Ventricle ; Ventricles (cerebral)</subject><ispartof>PloS one, 2014-11, Vol.9 (11), p.e113228-e113228</ispartof><rights>2014 Gangisetty 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 Gangisetty et al 2014 Gangisetty et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-2ba9e9b050da395598c65fe0ea5a1d0b7ad9b4746e0fc82cc6bfcbc15477e4b13</citedby><cites>FETCH-LOGICAL-c456t-2ba9e9b050da395598c65fe0ea5a1d0b7ad9b4746e0fc82cc6bfcbc15477e4b13</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/PMC4237387/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237387/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23849,27907,27908,53774,53776,79351,79352</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25409090$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Homberg, Judith</contributor><creatorcontrib>Gangisetty, Omkaram</creatorcontrib><creatorcontrib>Bekdash, Rola</creatorcontrib><creatorcontrib>Maglakelidze, George</creatorcontrib><creatorcontrib>Sarkar, Dipak K</creatorcontrib><title>Fetal alcohol exposure alters proopiomelanocortin gene expression and hypothalamic-pituitary-adrenal axis function via increasing MeCP2 expression in the hypothalamus</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Proopiomelanocortin (POMC) is a precursor gene of the neuropeptide β-endorphin in the hypothalamus and is known to regulate various physiological functions including stress response. Several recent reports showed that fetal alcohol exposure programs the hypothalamus to produce lower levels of POMC gene transcripts and to elevate the hypothalamic-pituitary-adrenal (HPA) axis response to stressful stimuli. We investigated the role of methyl CpG binding protein (MeCP2) in the effects of prenatal ethanol on POMC gene expression and hypothalamic-pituitary-adrenal (HPA) axis function. Pregnant Sprague Dawley rats were fed between GD 7 and 21 with a liquid diet containing 6.7% alcohol, pair-fed with isocaloric liquid diet, or fed ad libitum with rat chow, and their male offsprings were used at 60 days after birth in this study. Fetal alcohol exposure reduced the level of POMC mRNA, but increased the level of DNA methylation of this gene in the arcuate nucleus (ARC) of the hypothalamus where the POMC neuronal cell bodies are located. Fetal alcohol exposed rats showed a significant increase in MeCP2 protein levels in POMC cells, MeCP2 gene transcript levels as well as increased MeCP2 protein binding on the POMC promoter in the arcuate nucleus. Lentiviral delivery of MeCP2 shRNA into the third ventricle efficiently reduced MeCP2 expression and prevented the effect of prenatal ethanol on POMC gene expression in the arcuate nucleus. MeCP2-shRNA treatment also normalized the prenatal ethanol-induced increase in corticotropin releasing hormone (CRH) gene expression in the hypothalamus and elevated plasma adrenocorticotrophic hormone (ACTH) and corticosterone hormone responses to lipopolysaccharide (LPS) challenge. These results suggest that fetal alcohol programming of POMC gene may involve recruitment of MeCP2 on to the methylated promoter of the POMC gene to suppress POMC transcript levels and contribute to HPA axis dysregulation.</description><subject>Adrenocorticotropic hormone</subject><subject>Alcohol use</subject><subject>Alcoholic beverages</subject><subject>Animals</subject><subject>Arcuate nucleus</subject><subject>Arcuate Nucleus of Hypothalamus - metabolism</subject><subject>Biology and Life Sciences</subject><subject>Corticosterone</subject><subject>Corticotropin-releasing hormone</subject><subject>CpG islands</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Epigenetics</subject><subject>Ethanol</subject><subject>Ethanol - adverse effects</subject><subject>Exposure</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Hypothalamic-pituitary-adrenal axis</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Hypothalamus</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>MeCP2 protein</subject><subject>Methyl-CpG binding protein</subject><subject>Methyl-CpG-Binding Protein 2 - metabolism</subject><subject>Nuclei (cytology)</subject><subject>Pituitary</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>Plasmids</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - chemically induced</subject><subject>Prenatal Exposure Delayed Effects - genetics</subject><subject>Prenatal Exposure Delayed Effects - metabolism</subject><subject>Pro-Opiomelanocortin - genetics</subject><subject>Pro-Opiomelanocortin - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Proopiomelanocortin</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Transcription</subject><subject>Ventricle</subject><subject>Ventricles (cerebral)</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAUjBCIlsI_QBCJC5cs_ozjC1JVUahUBAc4W47zsuuV1w62U7V_iN-Jw26rLUI-2HqemffGnqp6jdEKU4E_bMMcvXarKXhYIYwpId2T6hRLSpqWIPr06HxSvUhpixCnXds-r04IZ0iWdVr9voSsXa2dCZvgaridQpojlEKGmOophjDZsAOnfTAhZuvrNXhYgBFSssHX2g_15m4KeaOd3lnTTDbPNut41-ghgl_kb22qx9mbvBBurK6tNxF0sn5df4WL7-RYsPTIGzjSnNPL6tmoXYJXh_2s-nn56cfFl-b62-eri_PrxjDe5ob0WoLsEUeDppJz2ZmWj4BAc40H1As9yJ4J1gIaTUeMafvR9AZzJgSwHtOz6u1ed3IhqcMTJ4VlhwRhknQFcbVHDEFv1RTtrhhVQVv1txDiWunyTMaBkqwzhg5oHDrCCJaSYjACGzlAGZO3Revjodvc72Aw4HPU7pHo4xtvN2odbhQjVNBOFIH3B4EYfs2QstrZZMCV34Iwl7lbIpBAki_O3v0D_b87tkeZGFKKMD4Mg5FaYnfPUkvs1CF2hfbm2MgD6T5n9A-EjNx8</recordid><startdate>20141119</startdate><enddate>20141119</enddate><creator>Gangisetty, Omkaram</creator><creator>Bekdash, Rola</creator><creator>Maglakelidze, George</creator><creator>Sarkar, Dipak K</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>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>20141119</creationdate><title>Fetal alcohol exposure alters proopiomelanocortin gene expression and hypothalamic-pituitary-adrenal axis function via increasing MeCP2 expression in the hypothalamus</title><author>Gangisetty, Omkaram ; Bekdash, Rola ; Maglakelidze, George ; Sarkar, Dipak K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-2ba9e9b050da395598c65fe0ea5a1d0b7ad9b4746e0fc82cc6bfcbc15477e4b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adrenocorticotropic hormone</topic><topic>Alcohol use</topic><topic>Alcoholic beverages</topic><topic>Animals</topic><topic>Arcuate nucleus</topic><topic>Arcuate Nucleus of Hypothalamus - metabolism</topic><topic>Biology and Life Sciences</topic><topic>Corticosterone</topic><topic>Corticotropin-releasing hormone</topic><topic>CpG islands</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>Epigenetics</topic><topic>Ethanol</topic><topic>Ethanol - adverse effects</topic><topic>Exposure</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Hypothalamic-pituitary-adrenal axis</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Hypothalamus</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>MeCP2 protein</topic><topic>Methyl-CpG binding protein</topic><topic>Methyl-CpG-Binding Protein 2 - metabolism</topic><topic>Nuclei (cytology)</topic><topic>Pituitary</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>Plasmids</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - chemically induced</topic><topic>Prenatal Exposure Delayed Effects - genetics</topic><topic>Prenatal Exposure Delayed Effects - metabolism</topic><topic>Pro-Opiomelanocortin - genetics</topic><topic>Pro-Opiomelanocortin - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Proopiomelanocortin</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Transcription</topic><topic>Ventricle</topic><topic>Ventricles (cerebral)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gangisetty, Omkaram</creatorcontrib><creatorcontrib>Bekdash, Rola</creatorcontrib><creatorcontrib>Maglakelidze, George</creatorcontrib><creatorcontrib>Sarkar, Dipak K</creatorcontrib><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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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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>Gangisetty, Omkaram</au><au>Bekdash, Rola</au><au>Maglakelidze, George</au><au>Sarkar, Dipak K</au><au>Homberg, Judith</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal alcohol exposure alters proopiomelanocortin gene expression and hypothalamic-pituitary-adrenal axis function via increasing MeCP2 expression in the hypothalamus</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-11-19</date><risdate>2014</risdate><volume>9</volume><issue>11</issue><spage>e113228</spage><epage>e113228</epage><pages>e113228-e113228</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Proopiomelanocortin (POMC) is a precursor gene of the neuropeptide β-endorphin in the hypothalamus and is known to regulate various physiological functions including stress response. Several recent reports showed that fetal alcohol exposure programs the hypothalamus to produce lower levels of POMC gene transcripts and to elevate the hypothalamic-pituitary-adrenal (HPA) axis response to stressful stimuli. We investigated the role of methyl CpG binding protein (MeCP2) in the effects of prenatal ethanol on POMC gene expression and hypothalamic-pituitary-adrenal (HPA) axis function. Pregnant Sprague Dawley rats were fed between GD 7 and 21 with a liquid diet containing 6.7% alcohol, pair-fed with isocaloric liquid diet, or fed ad libitum with rat chow, and their male offsprings were used at 60 days after birth in this study. Fetal alcohol exposure reduced the level of POMC mRNA, but increased the level of DNA methylation of this gene in the arcuate nucleus (ARC) of the hypothalamus where the POMC neuronal cell bodies are located. Fetal alcohol exposed rats showed a significant increase in MeCP2 protein levels in POMC cells, MeCP2 gene transcript levels as well as increased MeCP2 protein binding on the POMC promoter in the arcuate nucleus. Lentiviral delivery of MeCP2 shRNA into the third ventricle efficiently reduced MeCP2 expression and prevented the effect of prenatal ethanol on POMC gene expression in the arcuate nucleus. MeCP2-shRNA treatment also normalized the prenatal ethanol-induced increase in corticotropin releasing hormone (CRH) gene expression in the hypothalamus and elevated plasma adrenocorticotrophic hormone (ACTH) and corticosterone hormone responses to lipopolysaccharide (LPS) challenge. These results suggest that fetal alcohol programming of POMC gene may involve recruitment of MeCP2 on to the methylated promoter of the POMC gene to suppress POMC transcript levels and contribute to HPA axis dysregulation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25409090</pmid><doi>10.1371/journal.pone.0113228</doi><oa>free_for_read</oa></addata></record> |
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recordid | cdi_plos_journals_1980724928 |
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 | Adrenocorticotropic hormone Alcohol use Alcoholic beverages Animals Arcuate nucleus Arcuate Nucleus of Hypothalamus - metabolism Biology and Life Sciences Corticosterone Corticotropin-releasing hormone CpG islands Deoxyribonucleic acid DNA DNA Methylation Epigenetics Ethanol Ethanol - adverse effects Exposure Female Gene expression Gene Expression Regulation Hypothalamic-pituitary-adrenal axis Hypothalamo-Hypophyseal System - metabolism Hypothalamus Lipopolysaccharides Male MeCP2 protein Methyl-CpG binding protein Methyl-CpG-Binding Protein 2 - metabolism Nuclei (cytology) Pituitary Pituitary-Adrenal System - metabolism Plasmids Pregnancy Prenatal Exposure Delayed Effects - chemically induced Prenatal Exposure Delayed Effects - genetics Prenatal Exposure Delayed Effects - metabolism Pro-Opiomelanocortin - genetics Pro-Opiomelanocortin - metabolism Promoter Regions, Genetic Proopiomelanocortin Rats Rats, Sprague-Dawley Rodents Transcription Ventricle Ventricles (cerebral) |
title | Fetal alcohol exposure alters proopiomelanocortin gene expression and hypothalamic-pituitary-adrenal axis function via increasing MeCP2 expression in the hypothalamus |
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