{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T23:49:25Z","timestamp":1776383365889,"version":"3.51.2"},"reference-count":24,"publisher":"Cambridge University Press (CUP)","issue":"1","license":[{"start":{"date-parts":[[2022,6,24]],"date-time":"2022-06-24T00:00:00Z","timestamp":1656028800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["cambridge.org"],"crossmark-restriction":true},"short-container-title":["J Dev Orig Health Dis"],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Exposure to pregnancy complications, including preeclampsia (PE), has lifelong influences on offspring\u2019s health. We have previously reported that experimental PE, induced in mice by administration of adenoviral sFlt1 at gestational day 8.5 combined with LPS at day 10.5, results in symmetrical growth restriction in female and asymmetrical growth restriction in male offspring. Here, we characterize the molecular phenotype of the fetal brain and liver with respect to gene transcription and DNA methylation at the end of gestation.<\/jats:p><jats:p>In fetal brain and liver, expression and DNA methylation of several key regulatory genes is altered by PE exposure, mostly independent of fetal sex. These alterations point toward a decreased gluconeogenesis in the liver and stimulated neurogenesis in the brain, potentially affecting long-term brain and liver function. The observed sex-specific growth restriction pattern is not reflected in the molecular data, showing that PE, rather than tissue growth, drives the molecular phenotype of PE-exposed offspring.<\/jats:p>","DOI":"10.1017\/s2040174422000344","type":"journal-article","created":{"date-parts":[[2022,6,24]],"date-time":"2022-06-24T08:27:30Z","timestamp":1656059250000},"page":"146-151","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":10,"title":["Preeclampsia-induced alterations in brain and liver gene expression and DNA methylation patterns in fetal mice"],"prefix":"10.1017","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3518-0764","authenticated-orcid":false,"given":"Naomi","family":"Hofsink","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dorieke 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A.","family":"Scherjon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9305-4045","authenticated-orcid":false,"given":"Torsten","family":"Pl\u00f6sch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"56","published-online":{"date-parts":[[2022,6,24]]},"reference":[{"key":"S2040174422000344_ref5","doi-asserted-by":"publisher","DOI":"10.1016\/j.tins.2020.02.003"},{"key":"S2040174422000344_ref14","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00664.2003"},{"key":"S2040174422000344_ref3","doi-asserted-by":"publisher","DOI":"10.1242\/dmm.035980"},{"key":"S2040174422000344_ref8","doi-asserted-by":"publisher","DOI":"10.1042\/AN20110027"},{"key":"S2040174422000344_ref11","doi-asserted-by":"publisher","DOI":"10.1002\/hep.20362"},{"key":"S2040174422000344_ref13","doi-asserted-by":"publisher","DOI":"10.1186\/1477-7827-12-80"},{"key":"S2040174422000344_ref1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(10)60279-6"},{"key":"S2040174422000344_ref6","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijdevneu.2011.02.011"},{"key":"S2040174422000344_ref12","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.25276"},{"key":"S2040174422000344_ref9","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijdevneu.2014.07.008"},{"key":"S2040174422000344_ref10","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbi.2012.01.015"},{"key":"S2040174422000344_ref7","doi-asserted-by":"publisher","DOI":"10.1002\/glia.23079"},{"key":"S2040174422000344_ref16","doi-asserted-by":"publisher","DOI":"10.1249\/MSS.0000000000002040"},{"key":"S2040174422000344_ref21","doi-asserted-by":"publisher","DOI":"10.1111\/nyas.14458"},{"key":"S2040174422000344_ref20","doi-asserted-by":"publisher","DOI":"10.1016\/j.isci.2020.101183"},{"key":"S2040174422000344_ref2","doi-asserted-by":"publisher","DOI":"10.1095\/biolreprod.115.135780"},{"key":"S2040174422000344_ref17","doi-asserted-by":"publisher","DOI":"10.1016\/j.biochi.2008.03.009"},{"key":"S2040174422000344_ref15","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-020-76501-8"},{"key":"S2040174422000344_ref19","volume-title":"Endotext","author":"Woollett","year":"2000"},{"key":"S2040174422000344_ref4","doi-asserted-by":"publisher","DOI":"10.1055\/s-0031-1275516"},{"key":"S2040174422000344_ref18","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.117.10782"},{"key":"S2040174422000344_ref22","doi-asserted-by":"publisher","DOI":"10.1101\/lm.2213711"},{"key":"S2040174422000344_ref24","doi-asserted-by":"publisher","DOI":"10.1126\/science.1090842"},{"key":"S2040174422000344_ref23","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2010.11.006"}],"container-title":["Journal 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2022. Published by Cambridge University Press in association with International Society for Developmental Origins of Health and Disease","name":"copyright","label":"Copyright","group":{"name":"copyright_and_licensing","label":"Copyright and Licensing"}},{"value":"This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (https:\/\/creativecommons.org\/licenses\/by\/4.0\/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.","name":"license","label":"License","group":{"name":"copyright_and_licensing","label":"Copyright and Licensing"}},{"value":"This content has been made available to all.","name":"free","label":"Free to read"}]}}