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Related Concept Videos

Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...

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Related Experiment Video

Updated: Jun 6, 2026

Mouse In Vivo Placental Targeted CRISPR Manipulation
07:39

Mouse In Vivo Placental Targeted CRISPR Manipulation

Published on: April 14, 2023

Plac1 Ablation Disrupts Signaling Pathways Essential for Prenatal Development and Induces a Preeclampsia-associated

Suzanne Jackman1, Xiaoyuan Kong1, Yulan Piao2

  • 1Department of Pediatrics, University of South Florida, Morsani College of Medicine, Tampa, FL.

Biorxiv : the Preprint Server for Biology
|June 5, 2026
PubMed
Summary

Placental gene Plac1 is crucial for embryonic development. Its absence disrupts placental signaling, leading to cellular stress, immune activation, and increased risks for preeclampsia and fetal growth restriction.

Keywords:
Developmental Origins of Health and Disease (DOHaD)Plac1Rho GTPase signalingbirth defectsbrain developmentcardiovascular diseasefetal growth restriction (FGR)placental developmentpreeclampsia

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Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Published on: January 26, 2024

Area of Science:

  • Developmental biology
  • Genetics
  • Reproductive medicine

Background:

  • The X-linked gene Plac1 is vital for placental and embryonic development.
  • Understanding Plac1's regulatory role is key to deciphering placental dysfunction.

Purpose of the Study:

  • To investigate Plac1-regulated gene expression in a mouse model.
  • To identify molecular pathways affected by Plac1 deficiency.

Main Methods:

  • Utilized a Plac1 knockout (KO) mouse model.
  • Performed gene expression microarray analysis at embryonic day (E) 16.5 and E18.5.
  • Applied Gene Ontology (GO), KEGG, and Ingenuity Pathway Analysis (IPA) for data interpretation.

Main Results:

  • Plac1 deficiency significantly altered gene expression, with thousands of genes downregulated and upregulated at E16.5 and E18.5.
  • Downregulated genes were enriched in Rho GTPase and actin cytoskeleton signaling pathways crucial for trophoblast development and vasculogenesis.
  • Upregulated genes indicated immune activation and oxidative stress responses, alongside a developing preeclampsia signature.

Conclusions:

  • Plac1 is essential for maintaining placental structure and function through critical signaling pathways.
  • Plac1 absence disrupts these pathways, causing cellular stress, immune responses, and contributing to adverse pregnancy outcomes like preeclampsia and fetal growth restriction.
  • Findings align with the Developmental Origins of Health and Disease (DOHaD) framework, highlighting Plac1's impact on long-term health.