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.catalogadorjlo
dc.contributor.authorGonzález-Madrid, Enrique
dc.contributor.authorRangel-Ramírez, Ma. Andreina
dc.contributor.authorOpazo, María C.
dc.contributor.authorEspinoza Soto, Sebastián Andrés
dc.contributor.authorElgueta Bustos, Daniela Paz
dc.contributor.authorCancino Lobos, Gonzalo Ignacio
dc.contributor.authorMery, Elena
dc.contributor.authorArdiles, Álvaro O.
dc.contributor.authorDuarte, Luisa F.
dc.contributor.authorSoto, Jorge A.
dc.contributor.authorCarreño, Leandro J.
dc.contributor.authorSimon, Felipe
dc.contributor.authorBueno Ramírez, Susan Marcela
dc.contributor.authorGonzález Muñoz, Pablo Alberto
dc.contributor.authorKalergis Parra, Alexis Mikes
dc.contributor.authorRiedel, Claudia A.
dc.date.accessioned2025-12-04T13:48:46Z
dc.date.available2025-12-04T13:48:46Z
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.fechaingreso.objetodigital2025-12-04
dc.format.extent20 páginas
dc.fuente.origenORCID
dc.identifier.doi10.1038/s41598-025-26206-7
dc.identifier.issn2045-2322
dc.identifier.urihttps://doi.org/10.1038/s41598-025-26206-7
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/107259
dc.information.autorucFacultad de Ciencias Biológicas; Espinoza Soto, Sebastián Andrés; S/I; 179058
dc.information.autorucFacultad de Ciencias Biológicas; Elgueta Bustos, Daniela Paz; S/I; 149684
dc.information.autorucFacultad de Ciencias Biológicas; Cancino Lobos, Gonzalo; 0000-0001-8697-7282; 17709
dc.information.autorucFacultad de Ciencias Biológicas; Bueno Ramírez, Susan Marcela; 0000-0002-7551-8088; 113541
dc.information.autorucFacultad de Ciencias Biológicas; González Muñoz, Pablo Alberto; 0000-0001-7709-6870; 15616
dc.information.autorucFacultad de Ciencias Biológicas; Kalergis Parra, Alexis Mikes; 0000-0001-7622-5263; 90610
dc.language.isoen
dc.nota.accesocontenido completo
dc.revistaScientific Reports
dc.rightsacceso abierto
dc.subjectGestational hypothyroxinemia
dc.subjectPrenatal inflammation
dc.subjectCytokines
dc.subjectMaternal-fetal interface
dc.subjectEmbryonic neurodevelopment
dc.subject.ddc610
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleGestational hypothyroxinemia causes an inflammatory environment at maternal-fetal tissues and fetal brain with impaired hippocampal dendritic spine maturation in the offspring
dc.typeartículo
sipa.codpersvinculados179058
sipa.codpersvinculados149684
sipa.codpersvinculados17709
sipa.codpersvinculados113541
sipa.codpersvinculados15616
sipa.codpersvinculados90610
sipa.trazabilidadORCID;2025-12-01
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