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Related Experiment Video

Updated: Jan 31, 2026

Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
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Cell-Free DNA Release by Mouse Fetal Membranes.

Michala R Sawyer1, Sharareh Adeli1, Mark Phillippe2

  • 1Division of Maternal-Fetal Medicine and the Vincent Center for Reproductive Biology, Department of Obstetrics & Gynecology, Massachusetts General Hospital, 55 Fruit Street, Thier Bldg. 9-911, Boston, MA, 02114, USA.

Reproductive Sciences (Thousand Oaks, Calif.)
|December 22, 2018
PubMed
Summary

Mouse fetal membranes release cell-free DNA (cfDNA), which is hypomethylated and stimulates Toll-like receptor 9 (TLR9). This finding expands our understanding of cfDNA origins and immune signaling during pregnancy.

Keywords:
DNA methylationToll-like receptor 9apoptosisfetal cell-free DNAfetal membrane explants

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Area of Science:

  • Reproductive biology
  • Molecular biology
  • Immunology

Background:

  • Cell-free fetal DNA (cfDNA) originates from the placenta.
  • Fetal membranes also develop from the trophectoderm, suggesting they might also release cfDNA.

Purpose of the Study:

  • To investigate whether fetal membranes release cfDNA.
  • To characterize the properties and biological activity of cfDNA released from fetal membranes.

Main Methods:

  • Mouse fetal membranes were cultured with various stimuli (apoptosis inducers, inflammatory mediators).
  • cfDNA release, lactate dehydrogenase (LDH) levels, caspase activity, and protein expression were measured.
  • DNA methylation levels and cfDNA's effect on macrophage cytokine release were assessed.

Main Results:

  • Fetal membranes released cfDNA, with release levels correlating with LDH.
  • cfDNA release and caspase activity were modulated by apoptosis and inflammatory stimuli.
  • Released cfDNA was hypomethylated and stimulated interleukin-6 (IL6) release via Toll-like receptor 9 (TLR9).

Conclusions:

  • Mouse fetal membranes confirmed to release cfDNA.
  • The released cfDNA is hypomethylated.
  • cfDNA acts as a potent stimulator of TLR9, influencing immune responses.