DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases
Background Birthweight marks an important milestone of health across the lifespan, including cardiometabolic disease risk in later life. The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated w...
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| Veröffentlicht in: | Clinical epigenetics 2020-06, Vol.12 (1), p.1-78, Article 78 |
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| creator | Tekola-Ayele, Fasil Zeng, Xuehuo Ouidir, Marion Workalemahu, Tsegaselassie Zhang, Cuilin Delahaye, Fabien Wapner, Ronald |
| description | Background Birthweight marks an important milestone of health across the lifespan, including cardiometabolic disease risk in later life. The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated with birthweight can unravel genomic pathways that are dysregulated in aberrant fetal growth and cardiometabolic diseases in later life. Results We performed placental epigenome-wide association study (EWAS) of birthweight in an ethnic diverse cohort of pregnant women (n = 301). Methylation at 15 cytosine-(phosphate)-guanine sites (CpGs) was associated with birthweight (false discovery rate (FDR) < 0.05). Methylation at four (26.7%) CpG sites was associated with placental transcript levels of 15 genes (FDR < 0.05), including genes known to be associated with adult lipid traits, inflammation and oxidative stress. Increased methylation at cg06155341 was associated with higher birthweight and lower FOSL1 expression, and lower FOSL1 expression was correlated with higher birthweight. Given the role of the FOSL1 transcription factor in regulating developmental processes at the maternal-fetal interface, epigenetic mechanisms at this locus may regulate fetal development. We demonstrated trans-tissue portability of methylation at four genes (MLLT1, PDE9A, ASAP2, and SLC20A2) implicated in birthweight by a previous study in cord blood. We also found that methylation changes known to be related to maternal underweight, preeclampsia and adult type 2 diabetes were associated with lower birthweight in placenta. Conclusion We identified novel placental DNA methylation changes associated with birthweight. Placental epigenetic mechanisms may underlie dysregulated fetal development and early origins of adult cardiometabolic diseases. Clinical trial registration ClinicalTrials.gov, NCT00912132 Keywords: Placenta, Birthweight, Fetal growth, DNA methylation, Transcriptomics, Expression quantitative trait methylation (eQTM), Developmental origins of health and disease (DOHaD) |
| doi_str_mv | 10.1186/s13148-020-00873-x |
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The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated with birthweight can unravel genomic pathways that are dysregulated in aberrant fetal growth and cardiometabolic diseases in later life. Results We performed placental epigenome-wide association study (EWAS) of birthweight in an ethnic diverse cohort of pregnant women (n = 301). Methylation at 15 cytosine-(phosphate)-guanine sites (CpGs) was associated with birthweight (false discovery rate (FDR) < 0.05). Methylation at four (26.7%) CpG sites was associated with placental transcript levels of 15 genes (FDR < 0.05), including genes known to be associated with adult lipid traits, inflammation and oxidative stress. Increased methylation at cg06155341 was associated with higher birthweight and lower FOSL1 expression, and lower FOSL1 expression was correlated with higher birthweight. Given the role of the FOSL1 transcription factor in regulating developmental processes at the maternal-fetal interface, epigenetic mechanisms at this locus may regulate fetal development. We demonstrated trans-tissue portability of methylation at four genes (MLLT1, PDE9A, ASAP2, and SLC20A2) implicated in birthweight by a previous study in cord blood. We also found that methylation changes known to be related to maternal underweight, preeclampsia and adult type 2 diabetes were associated with lower birthweight in placenta. Conclusion We identified novel placental DNA methylation changes associated with birthweight. Placental epigenetic mechanisms may underlie dysregulated fetal development and early origins of adult cardiometabolic diseases. Clinical trial registration ClinicalTrials.gov, NCT00912132 Keywords: Placenta, Birthweight, Fetal growth, DNA methylation, Transcriptomics, Expression quantitative trait methylation (eQTM), Developmental origins of health and disease (DOHaD)</description><identifier>ISSN: 1868-7075</identifier><identifier>ISSN: 1868-7083</identifier><identifier>EISSN: 1868-7083</identifier><identifier>EISSN: 1868-7075</identifier><identifier>DOI: 10.1186/s13148-020-00873-x</identifier><identifier>PMID: 32493484</identifier><language>eng</language><publisher>London: BioMed Central Ltd</publisher><subject>Adults ; Biotechnology industries ; Birth weight ; Cord blood ; CpG islands ; Cytosine ; Deoxyribonucleic acid ; Diabetes mellitus (non-insulin dependent) ; DNA ; DNA methylation ; Epigenetic inheritance ; Epigenetics ; Fetal development ; Fetuses ; Gene expression ; Gene loci ; Genes ; Genetic aspects ; Genetic research ; Gestational age ; Guanine ; Kinases ; Life Sciences ; Life span ; Methylation ; Oxidative stress ; Phosphates ; Placenta ; Pre-eclampsia ; Pregnant women ; Pyrimidines ; Regression analysis ; Santé publique et épidémiologie ; Type 2 diabetes ; Underweight ; Womens health</subject><ispartof>Clinical epigenetics, 2020-06, Vol.12 (1), p.1-78, Article 78</ispartof><rights>COPYRIGHT 2020 BioMed Central Ltd.</rights><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-93610f93ddcb92e90d794c1643d9d4cff077334e19ef7e55dc81469b3608cca23</citedby><cites>FETCH-LOGICAL-c508t-93610f93ddcb92e90d794c1643d9d4cff077334e19ef7e55dc81469b3608cca23</cites><orcidid>0000-0003-4194-9370</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268466/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268466/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://hal.science/hal-04662406$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Tekola-Ayele, Fasil</creatorcontrib><creatorcontrib>Zeng, Xuehuo</creatorcontrib><creatorcontrib>Ouidir, Marion</creatorcontrib><creatorcontrib>Workalemahu, Tsegaselassie</creatorcontrib><creatorcontrib>Zhang, Cuilin</creatorcontrib><creatorcontrib>Delahaye, Fabien</creatorcontrib><creatorcontrib>Wapner, Ronald</creatorcontrib><title>DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases</title><title>Clinical epigenetics</title><description>Background Birthweight marks an important milestone of health across the lifespan, including cardiometabolic disease risk in later life. The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated with birthweight can unravel genomic pathways that are dysregulated in aberrant fetal growth and cardiometabolic diseases in later life. Results We performed placental epigenome-wide association study (EWAS) of birthweight in an ethnic diverse cohort of pregnant women (n = 301). Methylation at 15 cytosine-(phosphate)-guanine sites (CpGs) was associated with birthweight (false discovery rate (FDR) < 0.05). Methylation at four (26.7%) CpG sites was associated with placental transcript levels of 15 genes (FDR < 0.05), including genes known to be associated with adult lipid traits, inflammation and oxidative stress. Increased methylation at cg06155341 was associated with higher birthweight and lower FOSL1 expression, and lower FOSL1 expression was correlated with higher birthweight. Given the role of the FOSL1 transcription factor in regulating developmental processes at the maternal-fetal interface, epigenetic mechanisms at this locus may regulate fetal development. We demonstrated trans-tissue portability of methylation at four genes (MLLT1, PDE9A, ASAP2, and SLC20A2) implicated in birthweight by a previous study in cord blood. We also found that methylation changes known to be related to maternal underweight, preeclampsia and adult type 2 diabetes were associated with lower birthweight in placenta. Conclusion We identified novel placental DNA methylation changes associated with birthweight. Placental epigenetic mechanisms may underlie dysregulated fetal development and early origins of adult cardiometabolic diseases. Clinical trial registration ClinicalTrials.gov, NCT00912132 Keywords: Placenta, Birthweight, Fetal growth, DNA methylation, Transcriptomics, Expression quantitative trait methylation (eQTM), Developmental origins of health and disease (DOHaD)</description><subject>Adults</subject><subject>Biotechnology industries</subject><subject>Birth weight</subject><subject>Cord blood</subject><subject>CpG islands</subject><subject>Cytosine</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Fetal development</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Gene loci</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic research</subject><subject>Gestational age</subject><subject>Guanine</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Life span</subject><subject>Methylation</subject><subject>Oxidative stress</subject><subject>Phosphates</subject><subject>Placenta</subject><subject>Pre-eclampsia</subject><subject>Pregnant women</subject><subject>Pyrimidines</subject><subject>Regression analysis</subject><subject>Santé publique et épidémiologie</subject><subject>Type 2 diabetes</subject><subject>Underweight</subject><subject>Womens health</subject><issn>1868-7075</issn><issn>1868-7083</issn><issn>1868-7083</issn><issn>1868-7075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptksFuGyEQhldVqyZK8wI9IfXSHjaBBbNwqWQlbVPJai_tGWGY9RKx4AJ27BfocxfHUaJEhQNo5vt_GJimeU_wBSGCX2ZCCRMt7nCLsehpu3vVnNaEaHss6OvHfT87ac5zvsV1UCklwW-bE9oxSZlgp83f6x9zNEEZ914XFwPy0TjkAlp7bSAUjXTONaQLWHTnyoiWLpXxDtxqLEgHi2C3TpDzQRsHtIIAGSXwsNWhoCEmBDr5PbKwBR_XU_W8l2m78QVZl0FnyO-aN4P2Gc4f1rPm99cvv65u2sXPb9-v5ovWzLAoraSc4EFSa81SdiCx7SUzhDNqpWVmGHDfU8qASBh6mM2sEYRxuaQcC2N0R8-az0ff9WY5gT1UmLRX6-QmnfYqaqeeZ4Ib1SpuVd9xwTivBp-OBuML2c18oQ4xXKmOYb4llf34cFiKfzaQi5pcNuC9DhA3WVVMcioF7yv64QV6Gzcp1KeoVP1nITkRT9RKe1AuDLHe0RxM1Zx3PZWYzWilLv5D1WlhciYGGFyNPxN0R4FJMecEw2NhBKtDs6ljs6nabOq-2dSO_gMJjMaT</recordid><startdate>20200603</startdate><enddate>20200603</enddate><creator>Tekola-Ayele, Fasil</creator><creator>Zeng, Xuehuo</creator><creator>Ouidir, Marion</creator><creator>Workalemahu, Tsegaselassie</creator><creator>Zhang, Cuilin</creator><creator>Delahaye, Fabien</creator><creator>Wapner, Ronald</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4194-9370</orcidid></search><sort><creationdate>20200603</creationdate><title>DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases</title><author>Tekola-Ayele, Fasil ; Zeng, Xuehuo ; Ouidir, Marion ; Workalemahu, Tsegaselassie ; Zhang, Cuilin ; Delahaye, Fabien ; Wapner, Ronald</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-93610f93ddcb92e90d794c1643d9d4cff077334e19ef7e55dc81469b3608cca23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adults</topic><topic>Biotechnology industries</topic><topic>Birth weight</topic><topic>Cord blood</topic><topic>CpG islands</topic><topic>Cytosine</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Fetal development</topic><topic>Fetuses</topic><topic>Gene expression</topic><topic>Gene loci</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic research</topic><topic>Gestational age</topic><topic>Guanine</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Life span</topic><topic>Methylation</topic><topic>Oxidative stress</topic><topic>Phosphates</topic><topic>Placenta</topic><topic>Pre-eclampsia</topic><topic>Pregnant women</topic><topic>Pyrimidines</topic><topic>Regression analysis</topic><topic>Santé publique et épidémiologie</topic><topic>Type 2 diabetes</topic><topic>Underweight</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tekola-Ayele, Fasil</creatorcontrib><creatorcontrib>Zeng, Xuehuo</creatorcontrib><creatorcontrib>Ouidir, Marion</creatorcontrib><creatorcontrib>Workalemahu, Tsegaselassie</creatorcontrib><creatorcontrib>Zhang, Cuilin</creatorcontrib><creatorcontrib>Delahaye, Fabien</creatorcontrib><creatorcontrib>Wapner, Ronald</creatorcontrib><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 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>Medical 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>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical epigenetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tekola-Ayele, Fasil</au><au>Zeng, Xuehuo</au><au>Ouidir, Marion</au><au>Workalemahu, Tsegaselassie</au><au>Zhang, Cuilin</au><au>Delahaye, Fabien</au><au>Wapner, Ronald</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases</atitle><jtitle>Clinical epigenetics</jtitle><date>2020-06-03</date><risdate>2020</risdate><volume>12</volume><issue>1</issue><spage>1</spage><epage>78</epage><pages>1-78</pages><artnum>78</artnum><issn>1868-7075</issn><issn>1868-7083</issn><eissn>1868-7083</eissn><eissn>1868-7075</eissn><abstract>Background Birthweight marks an important milestone of health across the lifespan, including cardiometabolic disease risk in later life. The placenta, a transient organ at the maternal-fetal interface, regulates fetal growth. Identifying genetic loci where DNA methylation in placenta is associated with birthweight can unravel genomic pathways that are dysregulated in aberrant fetal growth and cardiometabolic diseases in later life. Results We performed placental epigenome-wide association study (EWAS) of birthweight in an ethnic diverse cohort of pregnant women (n = 301). Methylation at 15 cytosine-(phosphate)-guanine sites (CpGs) was associated with birthweight (false discovery rate (FDR) < 0.05). Methylation at four (26.7%) CpG sites was associated with placental transcript levels of 15 genes (FDR < 0.05), including genes known to be associated with adult lipid traits, inflammation and oxidative stress. Increased methylation at cg06155341 was associated with higher birthweight and lower FOSL1 expression, and lower FOSL1 expression was correlated with higher birthweight. Given the role of the FOSL1 transcription factor in regulating developmental processes at the maternal-fetal interface, epigenetic mechanisms at this locus may regulate fetal development. We demonstrated trans-tissue portability of methylation at four genes (MLLT1, PDE9A, ASAP2, and SLC20A2) implicated in birthweight by a previous study in cord blood. We also found that methylation changes known to be related to maternal underweight, preeclampsia and adult type 2 diabetes were associated with lower birthweight in placenta. Conclusion We identified novel placental DNA methylation changes associated with birthweight. Placental epigenetic mechanisms may underlie dysregulated fetal development and early origins of adult cardiometabolic diseases. Clinical trial registration ClinicalTrials.gov, NCT00912132 Keywords: Placenta, Birthweight, Fetal growth, DNA methylation, Transcriptomics, Expression quantitative trait methylation (eQTM), Developmental origins of health and disease (DOHaD)</abstract><cop>London</cop><pub>BioMed Central Ltd</pub><pmid>32493484</pmid><doi>10.1186/s13148-020-00873-x</doi><orcidid>https://orcid.org/0000-0003-4194-9370</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adults Biotechnology industries Birth weight Cord blood CpG islands Cytosine Deoxyribonucleic acid Diabetes mellitus (non-insulin dependent) DNA DNA methylation Epigenetic inheritance Epigenetics Fetal development Fetuses Gene expression Gene loci Genes Genetic aspects Genetic research Gestational age Guanine Kinases Life Sciences Life span Methylation Oxidative stress Phosphates Placenta Pre-eclampsia Pregnant women Pyrimidines Regression analysis Santé publique et épidémiologie Type 2 diabetes Underweight Womens health |
| title | DNA methylation loci in placenta associated with birthweight and expression of genes relevant for early development and adult diseases |
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