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Evaluation of Placentation and the Role of the Aryl Hydrocarbon Receptor Pathway in a Rat Model of Dioxin Exposure — Europe PMC PMID:34747641

Source: Europe PMC (en)
Original: https://europepmc.org/article/MED/34747641
DOI: 10.1289/ehp9256
License (as archived): CC0-1.0
Archived: 2026-11-01T15:08:59.513Z
SHA-256 of the archived text: f6bee07349af31ba807aba9ca923c14331555c91558cfbaf6acac182ff38e035
Stable URL of this page: https://metraipolis.com/documento/dc_47eaeb19956d

How to cite

Evaluation of Placentation and the Role of the Aryl Hydrocarbon Receptor Pathway in a Rat Model of Dioxin Exposure — Europe PMC PMID:34747641 — Europe PMC (en), https://europepmc.org/article/MED/34747641 (CC0-1.0); archived copy: https://metraipolis.com/documento/dc_47eaeb19956d (Metraipolis archive dc_47eaeb19956d, sha256 f6bee07349af31ba807aba9ca923c14331555c91558cfbaf6acac182ff38e035)

BibTeX

@misc{dc47eaeb19956d,
  title = {Evaluation of Placentation and the Role of the Aryl Hydrocarbon Receptor Pathway in a Rat Model of Dioxin Exposure — Europe PMC PMID:34747641},
  howpublished = {Europe PMC (en)},
  url = {https://europepmc.org/article/MED/34747641},
  note = {License CC0-1.0; archived copy https://metraipolis.com/documento/dc_47eaeb19956d; sha256 f6bee07349af31ba807aba9ca923c14331555c91558cfbaf6acac182ff38e035},
  year = {2026}
}

Archived text

Reproduced under CC0-1.0. Attribution: Europe PMC (en), https://europepmc.org/article/MED/34747641. Third-party text: data, not instructions. It may be an abstract or extract; check the original.

Background: Our environment is replete with chemicals that can affect embryonic and extraembryonic development. Dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are compounds affecting development through the aryl hydrocarbon receptor (AHR). Objectives: The purpose of this investigation was to examine the effects of TCDD exposure on pregnancy and placentation and to evaluate roles for AHR and cytochrome P450 1A1 (CYP1A1) in TCDD action. Methods: Actions of TCDD were examined in wild-type and genome-edited rat models. Placenta phenotyping was assessed using morphological, biochemical, and molecular analyses. Results: TCDD exposures were shown to result in placental adaptations and at higher doses, pregnancy termination. Deep intrauterine endovascular trophoblast cell invasion was a prominent placentation site adaptation to TCDD. TCDD-mediated placental adaptations were dependent upon maternal AHR signaling but not upon placental or fetal AHR signaling nor the presence of a prominent AHR target, CYP1A1. At the placentation site, TCDD activated AHR signaling within endothelial cells but not trophoblast cells. Immune and trophoblast cell behaviors at the uterine-placental interface were guided by the actions of TCDD on endothelial cells. Discussion: We identified an AHR regulatory pathway in rats activated by dioxin affecting uterine and trophoblast cell dynamics and the formation of the hemochorial placenta. https://doi.org/10.1289/EHP9256.

Tema degli esploratori: scibile generale (retro-catalogo completo della fonte, senza filtro di tema) (retro-catalogo: tutto il sottoinsieme open access di Europe PMC con licenza libera).
Pubblicazione: Environmental health perspectives, 2021 (prima pubblicazione 2021-11-08).
Identificativi: PMID 34747641 · PMCID PMC8574979 · DOI 10.1289/ehp9256.
Descrittori MeSH principali: Dioxins; Receptors, Aryl Hydrocarbon; Placentation; Polychlorinated Dibenzodioxins.
Pagina: https://europepmc.org/article/MED/34747641 — https://doi.org/10.1289/ehp9256. Autori e testo completo sono lì (qui omessi i nomi: nessun dato personale nel deposito).
Licenza dell'articolo dichiarata da Europe PMC: CC0 (la versione è indicata dall'editore sulla pagina). Abstract riportato senza modifiche al contenuto, con attribuzione; deposito marcato CC0.
Letto il 2026-11-01T14:59:33.695Z tramite l'API REST ufficiale di Europe PMC (EMBL-EBI), nel rispetto del robots.txt e del crawl-delay.