The inflammatory and oxidative phenotype of gestational diabetes is epigenetically transmitted to the offspring: role of methyltransferase MLL1-induced H3K4me3
Hyperglycaemia during gestational diabetes (GD) predisposes women and their offspring to later cardiometabolic disease. The hyperglycaemia-mediated epigenetic changes remain to be elucidated. Methyltransferase MLL1-induced trimethylation of histone 3 at lysine 4 (H3K4me3) activates inflammatory and...
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| creator | Di Pietrantonio, Nadia Sánchez-Ceinos, Julia Shumliakivska, Mariana Rakow, Alexander Mandatori, Domitilla Di Tomo, Pamela Formoso, Gloria Bonfini, Tiziana Baldassarre, Maria Pompea Antonia Sennström, Maria Almahmeed, Wael Pandolfi, Assunta Cosentino, Francesco |
| description | Hyperglycaemia during gestational diabetes (GD) predisposes women and their offspring to later cardiometabolic disease. The hyperglycaemia-mediated epigenetic changes remain to be elucidated. Methyltransferase MLL1-induced trimethylation of histone 3 at lysine 4 (H3K4me3) activates inflammatory and oxidative phenotype. This epigenetic mark in GD women and its transmission to the offspring were investigated.
Peripheral blood mononuclear cells (PBMC) were collected from GD and control (C) women and also from adolescents born to women of both groups. Endothelial human umbilical vein endothelial cells (HUVEC) and cord blood mononuclear cells (CBMC) were from umbilical cords. The NF-κBp65 and NOX4 expressions were investigated by reverse transcription quantitative polymerase chain reaction and immunofluorescence (IF). MLL1 and H3K4me3 were investigated by immunoblotting and IF. H3K4me3 on NF-κBp65 and NOX4 promoters was studied by chromatin immunoprecipitation. Superoxide anion generation was measured by electron spin resonance spectroscopy. Plasma cytokines were measured by enzyme-linked immunosorbent assay. To investigate the role of MLL1, HUVEC were exposed to inhibitor MM102 or siRNA transfection.
PBMC, CBMC, and HUVEC showed an increase of NF-κBp65, IL-6, ICAM-1, MCP-1, and VCAM-1 mRNAs. These findings were associated with H3K4me3 enrichment in the promoter of NF-κBp65. Elevated H3K4me3 and cytokine levels were observed in GD adolescents. MLL1 drives H3K4me3 not only on NF-kB p65, but also on NOX4 promoter. Inhibition of MLL1 blunted NF-κBp65 and NOX4 by modulating inflammatory and oxidative phenotype.
Such proof-of-concept study shows persistence of MLL1-dependent H3K4me3 in offspring born to GD women, suggesting an epigenetic-driven transmission of maternal phenotype. These findings may pave the way for pharmacological reprogramming of adverse histone modifications to mitigate abnormal phenotypes underlying early ASCVD. |
| doi_str_mv | 10.1093/eurheartj/ehae688 |
| format | Article |
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Peripheral blood mononuclear cells (PBMC) were collected from GD and control (C) women and also from adolescents born to women of both groups. Endothelial human umbilical vein endothelial cells (HUVEC) and cord blood mononuclear cells (CBMC) were from umbilical cords. The NF-κBp65 and NOX4 expressions were investigated by reverse transcription quantitative polymerase chain reaction and immunofluorescence (IF). MLL1 and H3K4me3 were investigated by immunoblotting and IF. H3K4me3 on NF-κBp65 and NOX4 promoters was studied by chromatin immunoprecipitation. Superoxide anion generation was measured by electron spin resonance spectroscopy. Plasma cytokines were measured by enzyme-linked immunosorbent assay. To investigate the role of MLL1, HUVEC were exposed to inhibitor MM102 or siRNA transfection.
PBMC, CBMC, and HUVEC showed an increase of NF-κBp65, IL-6, ICAM-1, MCP-1, and VCAM-1 mRNAs. These findings were associated with H3K4me3 enrichment in the promoter of NF-κBp65. Elevated H3K4me3 and cytokine levels were observed in GD adolescents. MLL1 drives H3K4me3 not only on NF-kB p65, but also on NOX4 promoter. Inhibition of MLL1 blunted NF-κBp65 and NOX4 by modulating inflammatory and oxidative phenotype.
Such proof-of-concept study shows persistence of MLL1-dependent H3K4me3 in offspring born to GD women, suggesting an epigenetic-driven transmission of maternal phenotype. These findings may pave the way for pharmacological reprogramming of adverse histone modifications to mitigate abnormal phenotypes underlying early ASCVD.</description><identifier>ISSN: 0195-668X</identifier><identifier>ISSN: 1522-9645</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehae688</identifier><identifier>PMID: 39471481</identifier><language>eng</language><publisher>England</publisher><subject>Adolescent ; Adult ; Diabetes, Gestational - genetics ; Diabetes, Gestational - metabolism ; Epigenesis, Genetic ; Female ; Fetal Blood - metabolism ; Histone-Lysine N-Methyltransferase - genetics ; Histone-Lysine N-Methyltransferase - metabolism ; Histones - metabolism ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Hyperglycemia - genetics ; Hyperglycemia - metabolism ; Leukocytes, Mononuclear - metabolism ; Myeloid-Lymphoid Leukemia Protein - genetics ; Myeloid-Lymphoid Leukemia Protein - metabolism ; NADPH Oxidase 4 - genetics ; NADPH Oxidase 4 - metabolism ; Oxidative Stress - genetics ; Oxidative Stress - physiology ; Phenotype ; Pregnancy ; Prenatal Exposure Delayed Effects - metabolism ; Transcription Factor RelA - metabolism</subject><ispartof>European heart journal, 2024-12, Vol.45 (48), p.5171</ispartof><rights>The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c221t-62734f015ae59e7e1275a113be9276e6dc713cd972483f6202c9b3e43d55b9fb3</cites><orcidid>0000-0002-6967-5685 ; 0000-0003-4135-7631</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39471481$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:159963065$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Di Pietrantonio, Nadia</creatorcontrib><creatorcontrib>Sánchez-Ceinos, Julia</creatorcontrib><creatorcontrib>Shumliakivska, Mariana</creatorcontrib><creatorcontrib>Rakow, Alexander</creatorcontrib><creatorcontrib>Mandatori, Domitilla</creatorcontrib><creatorcontrib>Di Tomo, Pamela</creatorcontrib><creatorcontrib>Formoso, Gloria</creatorcontrib><creatorcontrib>Bonfini, Tiziana</creatorcontrib><creatorcontrib>Baldassarre, Maria Pompea Antonia</creatorcontrib><creatorcontrib>Sennström, Maria</creatorcontrib><creatorcontrib>Almahmeed, Wael</creatorcontrib><creatorcontrib>Pandolfi, Assunta</creatorcontrib><creatorcontrib>Cosentino, Francesco</creatorcontrib><title>The inflammatory and oxidative phenotype of gestational diabetes is epigenetically transmitted to the offspring: role of methyltransferase MLL1-induced H3K4me3</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Hyperglycaemia during gestational diabetes (GD) predisposes women and their offspring to later cardiometabolic disease. The hyperglycaemia-mediated epigenetic changes remain to be elucidated. Methyltransferase MLL1-induced trimethylation of histone 3 at lysine 4 (H3K4me3) activates inflammatory and oxidative phenotype. This epigenetic mark in GD women and its transmission to the offspring were investigated.
Peripheral blood mononuclear cells (PBMC) were collected from GD and control (C) women and also from adolescents born to women of both groups. Endothelial human umbilical vein endothelial cells (HUVEC) and cord blood mononuclear cells (CBMC) were from umbilical cords. The NF-κBp65 and NOX4 expressions were investigated by reverse transcription quantitative polymerase chain reaction and immunofluorescence (IF). MLL1 and H3K4me3 were investigated by immunoblotting and IF. H3K4me3 on NF-κBp65 and NOX4 promoters was studied by chromatin immunoprecipitation. Superoxide anion generation was measured by electron spin resonance spectroscopy. Plasma cytokines were measured by enzyme-linked immunosorbent assay. To investigate the role of MLL1, HUVEC were exposed to inhibitor MM102 or siRNA transfection.
PBMC, CBMC, and HUVEC showed an increase of NF-κBp65, IL-6, ICAM-1, MCP-1, and VCAM-1 mRNAs. These findings were associated with H3K4me3 enrichment in the promoter of NF-κBp65. Elevated H3K4me3 and cytokine levels were observed in GD adolescents. MLL1 drives H3K4me3 not only on NF-kB p65, but also on NOX4 promoter. Inhibition of MLL1 blunted NF-κBp65 and NOX4 by modulating inflammatory and oxidative phenotype.
Such proof-of-concept study shows persistence of MLL1-dependent H3K4me3 in offspring born to GD women, suggesting an epigenetic-driven transmission of maternal phenotype. These findings may pave the way for pharmacological reprogramming of adverse histone modifications to mitigate abnormal phenotypes underlying early ASCVD.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Diabetes, Gestational - genetics</subject><subject>Diabetes, Gestational - metabolism</subject><subject>Epigenesis, Genetic</subject><subject>Female</subject><subject>Fetal Blood - metabolism</subject><subject>Histone-Lysine N-Methyltransferase - genetics</subject><subject>Histone-Lysine N-Methyltransferase - metabolism</subject><subject>Histones - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Hyperglycemia - genetics</subject><subject>Hyperglycemia - metabolism</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Myeloid-Lymphoid Leukemia Protein - genetics</subject><subject>Myeloid-Lymphoid Leukemia Protein - metabolism</subject><subject>NADPH Oxidase 4 - genetics</subject><subject>NADPH Oxidase 4 - metabolism</subject><subject>Oxidative Stress - genetics</subject><subject>Oxidative Stress - physiology</subject><subject>Phenotype</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - metabolism</subject><subject>Transcription Factor RelA - metabolism</subject><issn>0195-668X</issn><issn>1522-9645</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kUFv1DAQhS0EokvhB3BBPnIJ9diJY3NDFVDEIi5F4mY5yWTjktjBdoD8Gv4qaXfZ04yevvc0mkfIS2BvgGlxhUsc0MZ8d4WDRanUI7KDivNCy7J6THYMdFVIqb5fkGcp3THGlAT5lFwIXdZQKtiRv7cDUuf70U6TzSGu1PqOhj-us9n9QjoP6ENeZ6ShpwdMeZODtyPtnG0wY6IuUZzdAT1m19pxXGmO1qfJ5YwdzYHm4d7cpzk6f3hLYxgfwibMwzo-sD1Gm5B-2e-hcL5b2s14Iz6XE4rn5Elvx4QvTvOSfPvw_vb6pth__fjp-t2-aDmHXEhei7JnUFmsNNYIvK4sgGhQ81qi7NoaRNvpmpdK9JIz3upGYCm6qmp034hLUhxz02-cl8Zsx042riZYZ07Sj21Do5QCYBv_-sjPMfxctr-YyaUWx9F6DEsyAjiXfIPlhsIRbWNIKWJ_Dgdm7ns05x7NqcfN8-oUvzQTdmfH_-LEP-s3oPc</recordid><startdate>20241223</startdate><enddate>20241223</enddate><creator>Di Pietrantonio, Nadia</creator><creator>Sánchez-Ceinos, Julia</creator><creator>Shumliakivska, Mariana</creator><creator>Rakow, Alexander</creator><creator>Mandatori, Domitilla</creator><creator>Di Tomo, Pamela</creator><creator>Formoso, Gloria</creator><creator>Bonfini, Tiziana</creator><creator>Baldassarre, Maria Pompea Antonia</creator><creator>Sennström, Maria</creator><creator>Almahmeed, Wael</creator><creator>Pandolfi, Assunta</creator><creator>Cosentino, Francesco</creator><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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><orcidid>https://orcid.org/0000-0002-6967-5685</orcidid><orcidid>https://orcid.org/0000-0003-4135-7631</orcidid></search><sort><creationdate>20241223</creationdate><title>The inflammatory and oxidative phenotype of gestational diabetes is epigenetically transmitted to the offspring: role of methyltransferase MLL1-induced H3K4me3</title><author>Di Pietrantonio, Nadia ; Sánchez-Ceinos, Julia ; Shumliakivska, Mariana ; Rakow, Alexander ; Mandatori, Domitilla ; Di Tomo, Pamela ; Formoso, Gloria ; Bonfini, Tiziana ; Baldassarre, Maria Pompea Antonia ; Sennström, Maria ; Almahmeed, Wael ; Pandolfi, Assunta ; Cosentino, Francesco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c221t-62734f015ae59e7e1275a113be9276e6dc713cd972483f6202c9b3e43d55b9fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Diabetes, Gestational - genetics</topic><topic>Diabetes, Gestational - metabolism</topic><topic>Epigenesis, Genetic</topic><topic>Female</topic><topic>Fetal Blood - metabolism</topic><topic>Histone-Lysine N-Methyltransferase - genetics</topic><topic>Histone-Lysine N-Methyltransferase - metabolism</topic><topic>Histones - metabolism</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Hyperglycemia - genetics</topic><topic>Hyperglycemia - metabolism</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Myeloid-Lymphoid Leukemia Protein - genetics</topic><topic>Myeloid-Lymphoid Leukemia Protein - metabolism</topic><topic>NADPH Oxidase 4 - genetics</topic><topic>NADPH Oxidase 4 - metabolism</topic><topic>Oxidative Stress - genetics</topic><topic>Oxidative Stress - physiology</topic><topic>Phenotype</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - metabolism</topic><topic>Transcription Factor RelA - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Di Pietrantonio, Nadia</creatorcontrib><creatorcontrib>Sánchez-Ceinos, Julia</creatorcontrib><creatorcontrib>Shumliakivska, Mariana</creatorcontrib><creatorcontrib>Rakow, Alexander</creatorcontrib><creatorcontrib>Mandatori, Domitilla</creatorcontrib><creatorcontrib>Di Tomo, Pamela</creatorcontrib><creatorcontrib>Formoso, Gloria</creatorcontrib><creatorcontrib>Bonfini, Tiziana</creatorcontrib><creatorcontrib>Baldassarre, Maria Pompea Antonia</creatorcontrib><creatorcontrib>Sennström, Maria</creatorcontrib><creatorcontrib>Almahmeed, Wael</creatorcontrib><creatorcontrib>Pandolfi, Assunta</creatorcontrib><creatorcontrib>Cosentino, Francesco</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Di Pietrantonio, Nadia</au><au>Sánchez-Ceinos, Julia</au><au>Shumliakivska, Mariana</au><au>Rakow, Alexander</au><au>Mandatori, Domitilla</au><au>Di Tomo, Pamela</au><au>Formoso, Gloria</au><au>Bonfini, Tiziana</au><au>Baldassarre, Maria Pompea Antonia</au><au>Sennström, Maria</au><au>Almahmeed, Wael</au><au>Pandolfi, Assunta</au><au>Cosentino, Francesco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The inflammatory and oxidative phenotype of gestational diabetes is epigenetically transmitted to the offspring: role of methyltransferase MLL1-induced H3K4me3</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2024-12-23</date><risdate>2024</risdate><volume>45</volume><issue>48</issue><spage>5171</spage><pages>5171-</pages><issn>0195-668X</issn><issn>1522-9645</issn><eissn>1522-9645</eissn><abstract>Hyperglycaemia during gestational diabetes (GD) predisposes women and their offspring to later cardiometabolic disease. The hyperglycaemia-mediated epigenetic changes remain to be elucidated. Methyltransferase MLL1-induced trimethylation of histone 3 at lysine 4 (H3K4me3) activates inflammatory and oxidative phenotype. This epigenetic mark in GD women and its transmission to the offspring were investigated.
Peripheral blood mononuclear cells (PBMC) were collected from GD and control (C) women and also from adolescents born to women of both groups. Endothelial human umbilical vein endothelial cells (HUVEC) and cord blood mononuclear cells (CBMC) were from umbilical cords. The NF-κBp65 and NOX4 expressions were investigated by reverse transcription quantitative polymerase chain reaction and immunofluorescence (IF). MLL1 and H3K4me3 were investigated by immunoblotting and IF. H3K4me3 on NF-κBp65 and NOX4 promoters was studied by chromatin immunoprecipitation. Superoxide anion generation was measured by electron spin resonance spectroscopy. Plasma cytokines were measured by enzyme-linked immunosorbent assay. To investigate the role of MLL1, HUVEC were exposed to inhibitor MM102 or siRNA transfection.
PBMC, CBMC, and HUVEC showed an increase of NF-κBp65, IL-6, ICAM-1, MCP-1, and VCAM-1 mRNAs. These findings were associated with H3K4me3 enrichment in the promoter of NF-κBp65. Elevated H3K4me3 and cytokine levels were observed in GD adolescents. MLL1 drives H3K4me3 not only on NF-kB p65, but also on NOX4 promoter. Inhibition of MLL1 blunted NF-κBp65 and NOX4 by modulating inflammatory and oxidative phenotype.
Such proof-of-concept study shows persistence of MLL1-dependent H3K4me3 in offspring born to GD women, suggesting an epigenetic-driven transmission of maternal phenotype. These findings may pave the way for pharmacological reprogramming of adverse histone modifications to mitigate abnormal phenotypes underlying early ASCVD.</abstract><cop>England</cop><pmid>39471481</pmid><doi>10.1093/eurheartj/ehae688</doi><orcidid>https://orcid.org/0000-0002-6967-5685</orcidid><orcidid>https://orcid.org/0000-0003-4135-7631</orcidid></addata></record> |
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| ispartof | European heart journal, 2024-12, Vol.45 (48), p.5171 |
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| subjects | Adolescent Adult Diabetes, Gestational - genetics Diabetes, Gestational - metabolism Epigenesis, Genetic Female Fetal Blood - metabolism Histone-Lysine N-Methyltransferase - genetics Histone-Lysine N-Methyltransferase - metabolism Histones - metabolism Human Umbilical Vein Endothelial Cells - metabolism Humans Hyperglycemia - genetics Hyperglycemia - metabolism Leukocytes, Mononuclear - metabolism Myeloid-Lymphoid Leukemia Protein - genetics Myeloid-Lymphoid Leukemia Protein - metabolism NADPH Oxidase 4 - genetics NADPH Oxidase 4 - metabolism Oxidative Stress - genetics Oxidative Stress - physiology Phenotype Pregnancy Prenatal Exposure Delayed Effects - metabolism Transcription Factor RelA - metabolism |
| title | The inflammatory and oxidative phenotype of gestational diabetes is epigenetically transmitted to the offspring: role of methyltransferase MLL1-induced H3K4me3 |
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