Gestational diabetes impacts fetal precursor cell responses with potential consequences for offspring

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• dc.contributor.author Algaba-Chueca, Francisco
• dc.contributor.author Maymó-Masip, M.Elsa
• dc.contributor.author Ejarque, Miriam
• dc.contributor.author Ballesteros, Mónica
• dc.contributor.author Llauradó Cabot, Gemma
• dc.contributor.author López, Carlos
• dc.contributor.author Guarque, Albert
• dc.contributor.author Serena, Carolina
• dc.contributor.author Martínez-Guasch, Laia
• dc.contributor.author Gutiérrez, Cristina
• dc.contributor.author Bosch, Ramón
• dc.contributor.author Vendrell, Joan
• dc.contributor.author Megia, Ana
• dc.contributor.author Fernández Veledo, Sonia
• dc.date.accessioned 2020-06-22T06:33:35Z
• dc.date.available 2020-06-22T06:33:35Z
• dc.date.issued 2020
• dc.description.abstract Fetal programming has been proposed as a key mechanism underlying the association between intrauterine exposure to maternal diabetes and negative health outcomes in offspring. To determine whether gestational diabetes mellitus (GDM) might leave an imprint in fetal precursors of the amniotic membrane and whether it might be related to adverse outcomes in offspring, a prospective case-control study was conducted, in which amniotic mesenchymal stem cells (AMSCs) and resident macrophages were isolated from pregnant patients, with either GDM or normal glucose tolerance, scheduled for cesarean section. After characterization, functional characteristics of AMSCs were analyzed and correlated with anthropometrical and clinical variables from both mother and offspring. GDM-derived AMSCs displayed an impaired proliferation and osteogenic potential when compared with control cells, accompanied by superior invasive and chemotactic capacity. The expression of genes involved in the inflammatory response (TNFα, MCP-1, CD40, and CTSS) was upregulated in GDM-derived AMSCs, whereas anti-inflammatory IL-33 was downregulated. Macrophages isolated from the amniotic membrane of GDM mothers consistently showed higher expression of MCP-1 as well. In vitro studies in which AMSCs from healthy control women were exposed to hyperglycemia, hyperinsulinemia, and palmitic acid confirmed these results. Finally, genes involved in the inflammatory response were associated with maternal insulin sensitivity and prepregnancy body mass index, as well as with fetal metabolic parameters. These results suggest that the GDM environment could program stem cells and subsequently favor metabolic dysfunction later in life. Fetal adaptive programming in the setting of GDM might have a direct negative impact on insulin resistance of offspring.
• dc.format.mimetype application/pdf
• dc.identifier.citation Algaba-Chueca F, Maymó-Masip E, Ejarque M, Ballesteros M, Llauradó G, López C, et al. Gestational diabetes impacts fetal precursor cell responses with potential consequences for offspring. Stem Cells Transl Med. 2020 Mar; 9(3):351-363. DOI: 10.1002/sctm.19-0242
• dc.identifier.doi http://dx.doi.org/10.1002/sctm.19-0242
• dc.identifier.issn 2157-6564
• dc.identifier.uri http://hdl.handle.net/10230/45023
• dc.language.iso eng
• dc.publisher Wiley
• dc.rights Copyright © 2019 The Authors. STEM CELLS TRANSLATIONAL MEDICINE published by Wiley Periodicals, Inc. on behalf of AlphaMed Press. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• dc.subject.keyword Fetal precursors
• dc.subject.keyword Gestational diabetes
• dc.subject.keyword Offspring
• dc.subject.keyword Placenta
• dc.subject.keyword Programming
• dc.subject.keyword Stem cells
• dc.title Gestational diabetes impacts fetal precursor cell responses with potential consequences for offspring
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion