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Updated: May 21, 2025
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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
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Evidence for Complement Activation in Preeclampsia Placenta and Its Presence in Circulation.
Shibin Cheng1, Wendy Norris2, Satyan Kalkunte2,3
1Department of Pediatrics, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Summary
Preeclampsia involves increased complement activation and reduced protective proteins, leading to trophoblast cell death. Targeting complement pathways may offer new treatments for preeclampsia.
Area of Science:
- Immunology
- Reproductive Biology
- Pathophysiology
Background:
- Preeclampsia (PE) is a severe pregnancy disorder linked to placental issues, inflammation, and stress.
- Complement cascade activation is implicated in PE, but its direct impact on trophoblast health is unclear.
Purpose of the Study:
- To investigate complement activation and its effects on trophoblast cells in preeclampsia.
- To assess the role of complement regulatory proteins in preeclampsia pathogenesis.
Main Methods:
- Immunofluorescence detected membrane attack complex (MAC) deposition in placental tissues and trophoblast cells.
- Cell viability assays assessed trophoblast responses to normal (NP) and preeclamptic (PE) serum.
- Flow cytometry and immunohistochemistry quantified complement regulatory proteins (CD55, CD59, CD46).
Main Results:
- PE placentas showed increased MAC deposition and reduced CD55 expression compared to normal.
- PE serum induced cell death in specific trophoblast cells (TCL-1), which was prevented by complement inactivation.
- TCL-1 cells had lower CD55/CD59 expression, and blocking these proteins increased their susceptibility to PE serum.
Conclusions:
- Amplified complement activation and impaired regulation contribute to trophoblast cell death in PE.
- Targeting complement dysregulation presents a potential therapeutic strategy for preeclampsia.
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