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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Preeclampsia is associated with placental complement C4d deposition
E Pierik1, M H de Jong-Schoots2, M Bulthuis2
1Department of Obstetrics and Gynecology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Insights
Preeclampsia is linked to increased placental C4d deposition, especially in early-onset cases. This suggests the complement system plays a role in preeclampsia development, warranting further subtype-specific research.
Area of Science:
- Immunology
- Obstetrics
- Pathophysiology
Background:
- Preeclampsia poses significant risks to maternal and infant health.
- The role of the complement system in preeclampsia pathogenesis is not well understood.
- Immune factor alterations are implicated in preeclampsia, but complement system involvement requires further study.
Purpose of the Study:
- To investigate placental complement deposition differences in preeclampsia.
- To compare early-onset preeclampsia, late-onset preeclampsia, healthy term, and spontaneous preterm birth placentas.
- To examine the deposition of specific complement factors (C1q, C4d, C3d, C5b-9, CD59) in placental tissues.
Main Methods:
- Immunohistochemistry was used to analyze placental tissues.
- Placentas from early onset preeclampsia (n=26), late onset preeclampsia (n=26), healthy term controls (n=24), and spontaneous preterm births (n=14) were examined.
- Specific complement proteins (C1q, C4d, C3d, C5b-9, CD59) were targeted for deposition analysis.
Main Results:
- C4d deposition was found in trophoblasts of 25.5% of preeclampsia cases, significantly differing from healthy controls.
- Early-onset preeclampsia showed significantly higher C4d deposition compared to healthy term and spontaneous preterm births.
- No significant differences in C1q, C3d, C5b-9, or CD59 deposition were observed between the study groups.
Conclusions:
- Increased C4d deposition in early-onset preeclampsia placentas suggests a role for the complement system.
- These findings highlight the complexity of preeclampsia and the need for subtype-specific research.
- Further investigation into the complement system's involvement in preeclampsia pathophysiology is warranted.
Introduction:
Preeclampsia complicating pregnancy can be life-threatening for both mother and infant, often resulting in maternal and neonatal morbidity. Previous studies have related changes in specific immune factors to preeclampsia; however, the role of the complement system in preeclampsia remains understudied. Therefore, this study aims to examine differences in placental complement deposition in pregnancies complicated by preeclampsia and healthy term control pregnancies. In addition, we compared early and late preeclampsia with healthy term and spontaneous preterm births.
Methods:
Placentas from pregnancies complicated by early onset preeclampsia (n = 26), late onset preeclampsia (n = 26), healthy term controls (n = 24), and spontaneous preterm births (n = 14) were investigated for the presence of complement using immunohistochemistry for C1q, C4d, C3d, C5b-9, and CD59.
Results:
Deposition of C4d was observed at the trophoblast in 25.5 % of all preeclampsia cases and differed from healthy term controls (p = 0.029). C4d was observed in 12.0 % of late onset preeclampsia and 38.5 % of early onset preeclampsia placentas. None or minimal C4d was found in placentas of healthy term and preterm births. C4d trophoblast deposition significantly differed between early onset preeclampsia and healthy term (p = 0.002) and spontaneous preterm births (p = 0.022). With respect to C1q, C3d, C5b-9 and CD59, no significant differences were observed between the groups.
Conclusion:
Our data demonstrate an increase in C4d deposition in placentas of early onset preeclampsia compared to healthy term controls and spontaneous preterm births, suggesting a possible role for the complement system in preeclampsia. Our findings underscore the complexity of preeclampsia pathophysiology and highlight the need for more refined, subtype-specific investigations.
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