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Updated: Dec 30, 2025
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Isolation of Primary Human Decidual Cells from the Fetal Membranes of Term Placentae
Published on: April 30, 2018
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Thrombin-Induced Decidual Colony-Stimulating Factor-2 Promotes Abruption-Related Preterm Birth by Weakening Fetal
Rachel G Sinkey1, Ozlem Guzeloglu-Kayisli1, Sefa Arlier2
1Department of Obstetrics and Gynecology, University of South Florida, Morsani College of Medicine, Tampa, Florida.
The American Journal of Pathology
|January 21, 2020
Summary
Thrombin increases colony-stimulating factor-2 (CSF-2) in decidual cells, weakening fetal membranes and potentially causing preterm premature rupture of membranes (PPROM). Medroxyprogesterone acetate (MPA) can inhibit this effect.
Area of Science:
- Reproductive Biology
- Obstetrics
- Cell Signaling
Background:
- Preterm premature rupture of membranes (PPROM) and abruptions are linked to thrombin generation and unclear mechanisms.
- Decidual cell-expressed tissue factor plays a role in these pregnancy complications.
Purpose of the Study:
- To investigate the hypothesis that thrombin-induced colony-stimulating factor-2 (CSF-2) in decidual cells promotes fetal membrane weakening and PPROM.
- To examine the role of CSF-2 paracrine signaling via its receptor (CSF2R) in trophoblasts.
Main Methods:
- Immunostaining of decidua basalis sections from term, idiopathic preterm birth, and abruption-complicated pregnancies for CSF-2.
- Real-time quantitative PCR to measure CSF2 and CSF2R mRNA levels in decidual and trophoblast cells.
- In vitro experiments treating term decidual cell monolayers with thrombin and MPA, followed by analysis of conditioned media effects on fetal membrane weakening.
Main Results:
- CSF-2 immunoreactivity was significantly higher in abruption-complicated and idiopathic preterm birth specimens compared to term specimens.
- CSF2 mRNA was higher in decidual cells, while CSF2R mRNA was significantly higher in trophoblasts.
- Thrombin increased CSF-2 secretion in decidual cells, leading to fetal membrane weakening, an effect inhibited by MPA.
Conclusions:
- Decidual cell-derived CSF-2, acting through trophoblast CSF2R, contributes to thrombin-induced fetal membrane weakening.
- This pathway is implicated in the pathogenesis of abruption-related PPROM and preterm birth.
- MPA demonstrates a potential inhibitory role in this process.
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