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Updated: Apr 19, 2026

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
MFG-E8 inhibits AT1-AA production to alleviate preeclampsia
Fengfeng Xie1, Zhanhua Shi1, Jiaying Zhu2
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Purpose:
Preeclampsia (PE) is a multifactorial disease, in which immune dysregulations especially pathogenic autoantibody AT1-AA is critically involved. MFG-E8 deficiency can lead to autoimmune disorders, yet its role in AT1-AA-mediated PE remains unclear. Thus, this study explores whether MFG-8 inhibits AT1-AA production by promoting macrophage phagocytosis of apoptosis trophoblasts.
Methods:
Placental MFG-E8 expression, trophoblast apoptosis, and serum levels of TNF-α, sFlt-1, and AT1-AA were detected between PE patients and healthy subjects. The LPS-induced PE rat models and trophoblast-macrophage co-culture system were established to evaluate the effects of MFG-E8 on AT1-AA production and macrophage phagocytic function.
Results:
Reduced placental MFG-E, increased trophoblast apoptosis, and elevated serum levels of TNF-α, sFlt-1, and AT1-AA were detected in PE patients. MFG-E8 administration attenuated PE symptoms in rats, reduced AT1-AA expressions, and promoted macrophage clearance of apoptotic trophoblasts and AT1R antigen in vitro.
Conclusion:
MFG-E8 alleviates PE progression by promoting macrophage phagocytosis of apoptotic trophoblasts and inhibiting AT1-AA production.
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