Methylation changes and pathways affected in preterm birth: a role for SLC6A3 in neurodevelopment
To analyze whether preterm newborns show differences in methylation patterns in comparison to full-term newborns in white blood cells. Anthropometrical, biochemical features and methylation levels of preterm newborns (n = 24) and full-term newborns (n = 22) recruited in La Paz University Hospital (S...
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| Veröffentlicht in: | Epigenomics 2018-01, Vol.10 (1), p.91-103 |
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| creator | Arpón, Ana Milagro, Fermín I Laja, Ana Segura, Víctor de Pipaón, Miguel Sáenz Riezu-Boj, José-Ignacio Alfredo Martínez, J |
| description | To analyze whether preterm newborns show differences in methylation patterns in comparison to full-term newborns in white blood cells.
Anthropometrical, biochemical features and methylation levels of preterm newborns (n = 24) and full-term newborns (n = 22) recruited in La Paz University Hospital (Spain) were assessed at 12 months of gestational age, whereas Bayley Scale of Infant Development was evaluated at 24/36 months.
From all the statistically significant CpGs, methylation levels of cg00997378 (SLC6A3 gene) showed the highest differences (p |
| doi_str_mv | 10.2217/epi-2017-0082 |
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Anthropometrical, biochemical features and methylation levels of preterm newborns (n = 24) and full-term newborns (n = 22) recruited in La Paz University Hospital (Spain) were assessed at 12 months of gestational age, whereas Bayley Scale of Infant Development was evaluated at 24/36 months.
From all the statistically significant CpGs, methylation levels of cg00997378 (SLC6A3 gene) showed the highest differences (p < 0.0001), being associated with prematurity risk factors.
SLC6A3 methylation, previously related to attention-deficit/hyperactivity disorder, neuronal function and behavior, might be a potential epigenetic biomarker with value in the early diagnosis and management of neurodevelopmental diseases in newborns.</description><identifier>ISSN: 1750-1911</identifier><identifier>EISSN: 1750-192X</identifier><identifier>DOI: 10.2217/epi-2017-0082</identifier><identifier>PMID: 29172706</identifier><language>eng</language><publisher>England: Future Medicine Ltd</publisher><subject>Attention deficit hyperactivity disorder ; Biomarkers ; Chronic illnesses ; CpG Islands ; DNA Methylation ; Dopamine Plasma Membrane Transport Proteins - genetics ; Epigenetics ; Female ; Gestational age ; Humans ; Hyperactivity ; Infant, Premature ; Leukocytes ; Leukocytes - metabolism ; Male ; Neonates ; Nervous System - growth & development ; Neurodevelopmental disorders ; Nutrition ; Premature birth ; Risk analysis ; Risk factors ; Statistical analysis</subject><ispartof>Epigenomics, 2018-01, Vol.10 (1), p.91-103</ispartof><rights>Copyright Future Medicine Ltd Jan 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c321t-7ca8de6bcf2ac399a0df76a94faa5d4b03f594103c94af1ffb2673552bb8a6723</citedby><cites>FETCH-LOGICAL-c321t-7ca8de6bcf2ac399a0df76a94faa5d4b03f594103c94af1ffb2673552bb8a6723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2216527887/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2216527887?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>315,781,785,21391,27926,27927,33532,33533,43661,64387,64389,64391,72471,74106</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29172706$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arpón, Ana</creatorcontrib><creatorcontrib>Milagro, Fermín I</creatorcontrib><creatorcontrib>Laja, Ana</creatorcontrib><creatorcontrib>Segura, Víctor</creatorcontrib><creatorcontrib>de Pipaón, Miguel Sáenz</creatorcontrib><creatorcontrib>Riezu-Boj, José-Ignacio</creatorcontrib><creatorcontrib>Alfredo Martínez, J</creatorcontrib><title>Methylation changes and pathways affected in preterm birth: a role for SLC6A3 in neurodevelopment</title><title>Epigenomics</title><addtitle>Epigenomics</addtitle><description>To analyze whether preterm newborns show differences in methylation patterns in comparison to full-term newborns in white blood cells.
Anthropometrical, biochemical features and methylation levels of preterm newborns (n = 24) and full-term newborns (n = 22) recruited in La Paz University Hospital (Spain) were assessed at 12 months of gestational age, whereas Bayley Scale of Infant Development was evaluated at 24/36 months.
From all the statistically significant CpGs, methylation levels of cg00997378 (SLC6A3 gene) showed the highest differences (p < 0.0001), being associated with prematurity risk factors.
SLC6A3 methylation, previously related to attention-deficit/hyperactivity disorder, neuronal function and behavior, might be a potential epigenetic biomarker with value in the early diagnosis and management of neurodevelopmental diseases in newborns.</description><subject>Attention deficit hyperactivity disorder</subject><subject>Biomarkers</subject><subject>Chronic illnesses</subject><subject>CpG Islands</subject><subject>DNA Methylation</subject><subject>Dopamine Plasma Membrane Transport Proteins - genetics</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gestational age</subject><subject>Humans</subject><subject>Hyperactivity</subject><subject>Infant, Premature</subject><subject>Leukocytes</subject><subject>Leukocytes - metabolism</subject><subject>Male</subject><subject>Neonates</subject><subject>Nervous System - growth & development</subject><subject>Neurodevelopmental disorders</subject><subject>Nutrition</subject><subject>Premature birth</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Statistical analysis</subject><issn>1750-1911</issn><issn>1750-192X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</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><recordid>eNpd0E1r3DAQgGERGpKQ5thrEfTSixNptJas3sKSNoENOSSB3sxYHnUdbMuV5JT99_U2H4fqIg08DOJl7JMU5wDSXNDUFSCkKYSo4ICdSFOKQlr4-eH9LeUxO0vpSSxHQWW1PGLHYKUBI_QJw1vK212PuQsjd1scf1HiOLZ8wrz9g7tl8J5cppZ3I58iZYoDb7qYt9848hh64j5Efr9Z60u1NyPNMbT0TH2YBhrzR3bosU909nqfssfvVw_r62Jz9-NmfbkpnAKZC-Owakk3zgM6ZS2K1huNduURy3bVCOVLu5JCObtCL71vQBtVltA0FWoD6pR9fdk7xfB7ppTroUuO-h5HCnOqpdXWAsA_-uU_-hTmOC6_q5esugRTVWZRxYtyMaQUyddT7AaMu1qKvTP1kr_e56_3-Rf_-XXr3AzUvuu32Oov5uKAAQ</recordid><startdate>201801</startdate><enddate>201801</enddate><creator>Arpón, Ana</creator><creator>Milagro, Fermín I</creator><creator>Laja, Ana</creator><creator>Segura, Víctor</creator><creator>de Pipaón, Miguel Sáenz</creator><creator>Riezu-Boj, José-Ignacio</creator><creator>Alfredo Martínez, J</creator><general>Future Medicine Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>EHMNL</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>201801</creationdate><title>Methylation changes and pathways affected in preterm birth: a role for SLC6A3 in neurodevelopment</title><author>Arpón, Ana ; Milagro, Fermín I ; Laja, Ana ; Segura, Víctor ; de Pipaón, Miguel Sáenz ; Riezu-Boj, José-Ignacio ; Alfredo Martínez, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c321t-7ca8de6bcf2ac399a0df76a94faa5d4b03f594103c94af1ffb2673552bb8a6723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Attention deficit hyperactivity disorder</topic><topic>Biomarkers</topic><topic>Chronic illnesses</topic><topic>CpG Islands</topic><topic>DNA Methylation</topic><topic>Dopamine Plasma Membrane Transport Proteins - genetics</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gestational age</topic><topic>Humans</topic><topic>Hyperactivity</topic><topic>Infant, Premature</topic><topic>Leukocytes</topic><topic>Leukocytes - metabolism</topic><topic>Male</topic><topic>Neonates</topic><topic>Nervous System - growth & development</topic><topic>Neurodevelopmental disorders</topic><topic>Nutrition</topic><topic>Premature birth</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Statistical analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arpón, Ana</creatorcontrib><creatorcontrib>Milagro, Fermín I</creatorcontrib><creatorcontrib>Laja, Ana</creatorcontrib><creatorcontrib>Segura, Víctor</creatorcontrib><creatorcontrib>de Pipaón, Miguel Sáenz</creatorcontrib><creatorcontrib>Riezu-Boj, José-Ignacio</creatorcontrib><creatorcontrib>Alfredo Martínez, J</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>UK & Ireland Database</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>Medical Database</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</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>MEDLINE - Academic</collection><jtitle>Epigenomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arpón, Ana</au><au>Milagro, Fermín I</au><au>Laja, Ana</au><au>Segura, Víctor</au><au>de Pipaón, Miguel Sáenz</au><au>Riezu-Boj, José-Ignacio</au><au>Alfredo Martínez, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylation changes and pathways affected in preterm birth: a role for SLC6A3 in neurodevelopment</atitle><jtitle>Epigenomics</jtitle><addtitle>Epigenomics</addtitle><date>2018-01</date><risdate>2018</risdate><volume>10</volume><issue>1</issue><spage>91</spage><epage>103</epage><pages>91-103</pages><issn>1750-1911</issn><eissn>1750-192X</eissn><abstract>To analyze whether preterm newborns show differences in methylation patterns in comparison to full-term newborns in white blood cells.
Anthropometrical, biochemical features and methylation levels of preterm newborns (n = 24) and full-term newborns (n = 22) recruited in La Paz University Hospital (Spain) were assessed at 12 months of gestational age, whereas Bayley Scale of Infant Development was evaluated at 24/36 months.
From all the statistically significant CpGs, methylation levels of cg00997378 (SLC6A3 gene) showed the highest differences (p < 0.0001), being associated with prematurity risk factors.
SLC6A3 methylation, previously related to attention-deficit/hyperactivity disorder, neuronal function and behavior, might be a potential epigenetic biomarker with value in the early diagnosis and management of neurodevelopmental diseases in newborns.</abstract><cop>England</cop><pub>Future Medicine Ltd</pub><pmid>29172706</pmid><doi>10.2217/epi-2017-0082</doi><tpages>13</tpages></addata></record> |
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| subjects | Attention deficit hyperactivity disorder Biomarkers Chronic illnesses CpG Islands DNA Methylation Dopamine Plasma Membrane Transport Proteins - genetics Epigenetics Female Gestational age Humans Hyperactivity Infant, Premature Leukocytes Leukocytes - metabolism Male Neonates Nervous System - growth & development Neurodevelopmental disorders Nutrition Premature birth Risk analysis Risk factors Statistical analysis |
| title | Methylation changes and pathways affected in preterm birth: a role for SLC6A3 in neurodevelopment |
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