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Gestational hypothyroxinemia causes an inflammatory environment at maternal-fetal tissues and fetal brain with impaired hippocampal dendritic spine maturation in the offspring

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dc.contributor.authorGonzález, Enrique
dc.contributor.authorRangel, Andreina
dc.contributor.authorOpazo, María
dc.contributor.authorEspinoza, Sebastián
dc.contributor.authorElgueta, Daniela
dc.contributor.authorCancino, Gonzalo
dc.contributor.authorMery, Elena
dc.contributor.authorArdiles, Álvaro
dc.contributor.authorDuarte, Luisa
dc.contributor.authorSoto, Jorge
dc.contributor.authorCarreño, Leandro
dc.contributor.authorSimon, Felipe
dc.contributor.authorBueno, Susan
dc.contributor.authorGonzález, Pablo
dc.contributor.authorKalergis, Alexis
dc.date.accessioned2026-09-08T15:38:21Z
dc.date.available2026-09-08T15:38:21Z
dc.date.issued2025
dc.description.abstractGestational hypothyroxinemia (HTX) is associated with cognitive impairments and autism traits in offspring. However, the underlying mechanisms remain unclear. Prenatal inflammation impairs cortical development and induces diverse neurodevelopmental outcomes. Since thyroid dysfunction elicits inflammation, we sought to investigate whether HTX triggers prenatal pro-inflammatory responses. Using a mouse model of gestational HTX, we found elevated levels of IL-6 and IL-17 A in maternal serum, placental tissues, and embryonic brains at embryonic day (E)14 compared to euthyroid (EUT) dams. We also found increased proportions of dendritic cells, NK cells, M1-like macrophages, and monocytes in the placental tissues of HTX dams. Furthermore, gestational HTX exposure led to reduced Tbr2⁺ progenitors, increased Tbr1⁺ neurons, and an expanded Iba1⁺ microglial population in HTX-exposed embryos compared to EUT-exposed embryos. At postnatal day (P)55, the offspring gestated under HTX exhibited reduced hippocampal dendritic spine density and maturity compared to the progeny gestated under EUT. Notably, restoring T4 levels during HTX induction (HTX + T4 dams) prevented these alterations during pregnancy and in the offspring of HTX + T4 dams. These findings show that gestational HTX causes inflammation during pregnancy and has neurodevelopmental effects on the progeny, opening new pathways related to how maternal HTX impairs neurodevelopment in the offspring.
dc.description.versionVersión Publicada
dc.identifier.citationGonzález-Madrid E, Rangel-Ramírez MA, Opazo MC, Espinoza SA, Elgueta D, Cancino GI, Mery E, Ardiles ÁO, Duarte LF, Soto JA, Carreño LJ, Simon F, Bueno SM, González PA, Kalergis AM, Riedel CA. Gestational hypothyroxinemia causes an inflammatory environment at maternal-fetal tissues and fetal brain with impaired hippocampal dendritic spine maturation in the offspring. Sci Rep. 2025 Nov 26;15(1):42160. doi: 10.1038/s41598-025-26206-7
dc.identifier.doihttps://doi.org/10.1038/s41598-025-26206-7
dc.identifier.urihttps://hdl.handle.net/11447/11088
dc.language.isoen
dc.subjectCytokines
dc.subjectEmbryonic neurodevelopment
dc.subjectGestational hypothyroxinemia
dc.subjectHippocampal dendritic spines
dc.subjectMaternal-fetal interface
dc.subjectMicroglia
dc.subjectPrenatal inflammation
dc.titleGestational hypothyroxinemia causes an inflammatory environment at maternal-fetal tissues and fetal brain with impaired hippocampal dendritic spine maturation in the offspring
dc.typeArticle
dcterms.accessRightsAcceso Abierto
dcterms.sourceScientific reports
dspace.entity.typePublication

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