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Updated: May 2, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

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Type I interferon alters invasive extravillous trophoblast function.

Michael K Simoni, Seble G Negatu, Ju Young Park

Biorxiv : the Preprint Server for Biology

|April 1, 2024

Summary

Excessive type I interferon (IFN) signaling impairs embryo implantation by hindering trophoblast cell invasion and vascular remodeling. This disruption is linked to preeclampsia, a serious pregnancy complication.

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In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines

Published on: March 5, 2019

Area of Science:

Reproductive biology
Immunology
Developmental biology

Background:

Inappropriate type I interferon (IFN) signaling is implicated in poor pregnancy outcomes.
Understanding IFN's role in embryo implantation and placentation is crucial for maternal health.

Approach:

Utilized a biomimetic organ-on-a-chip model for human implantation.
Investigated the effects of elevated type I IFN exposure on extravillous trophoblast (EVT) function.
Performed single-cell transcriptome analysis to uncover molecular mechanisms.

Key Points:

Type I IFN exposure reduced EVT invasion capacity and endovascular emergence.
IFN signaling stunted EVT epithelial-to-mesenchymal transition, a process linked to preeclampsia pathogenesis.
Unwarranted IFN stimulation induced preeclampsia risk genes and a preeclamptic signature in EVTs.
Dysregulated EVT function led to diminished vascular remodeling.

Conclusions:

Type I IFN signaling disrupts EVT epithelial-to-mesenchymal transition, impacting spiral artery remodeling.
Abnormal EVT function induced by IFN may contribute to the development of preeclampsia.
This study implicates type I IFN as a potential maternal factor triggering preeclampsia.