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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
Increased platelet activation and thrombo-inflammation in early and late-onset preeclampsia
Kunal Singh1,2, Massimiliano Lia2,3, Akshay Prakasan Sheeja1
1Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics, University Hospital Leipzig, Leipzig University, Germany.
Insights
Thrombo-inflammation mechanisms differ between early- and late-onset preeclampsia. Maternal platelet activation is key in late-onset preeclampsia, suggesting distinct pathways in disease progression.
Area of Science:
- Obstetrics and Gynecology
- Vascular Biology
- Immunology
Background:
- Preeclampsia is a pregnancy complication characterized by hypertension and elevated sFlt-1/PlGF.
- It presents as early-onset (E-PE) or late-onset (L-PE) preeclampsia.
- Thrombo-inflammation, involving platelet activation and sterile inflammation, is implicated in preeclampsia pathophysiology, but differential regulation in E-PE vs. L-PE is unclear.
Purpose of the Study:
- To investigate the distinct roles of maternal platelet activation, inflammation, and endothelial dysfunction in E-PE versus L-PE.
Main Methods:
- Flow cytometry analyzed platelet activation markers (P-selectin, active αIIbβ3) in whole blood.
- Plasma levels of interleukin-1β (IL-1β) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured.
Main Results:
- Both E-PE and L-PE showed increased platelet activation and elevated plasma IL-1β and sVCAM-1 compared to controls.
- Maternal platelet activation correlated with disease severity and inflammatory markers specifically in L-PE.
- No significant correlation was found between αIIbβ3 expression and sFlt-1, IL-1β, or sVCAM-1.
Conclusions:
- Thrombo-inflammation is differentially regulated in L-PE and E-PE.
- Maternal factors, such as platelet activation, appear to play a significant role in L-PE pathophysiology.
- Further research with larger cohorts is needed to fully understand these mechanistic differences.
Background:
Preeclampsia is a vascular complication of pregnancy with limited therapeutic options. It is associated with hypertension and an increase in angiogenic factor soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor. Based on its onset, preclampsia can be categorized into early-onset (E-PE) or late-onset (L-PE) preeclampsia. Thrombo-inflammation, hallmarked by maternal platelet activation and sterile inflammation, is associated with pathophysiology of preeclampsia. However, whether these mechanisms are differentially regulated in E-PE vs L-PE remains unknown.
Objectives:
We aim to study the role of maternal platelet activation, inflammation and endothelial dysfunction in E-PE vs L-PE.
Methods:
Flow-cytometry analysis of platelet activation (P-selectin and active αIIbβ3) was conducted in whole blood from pregnant women with E-PE, L-PE and gestational age-matched patients. Plasma was evaluated for interleukin (IL)-1β and soluble vascular cell adhesion molecule 1 (sVCAM-1).
Results:
An increase in P-selectin and active αIIbβ3 expressing platelets in both forms of preeclampsia (n = 22) was observed compared with their gestational age-matched controls (n = 18). Similarly, an increase in plasma IL-1β and sVCAM-1 was observed in both forms of preeclampsia, suggesting inflammation and endothelial dysfunction, respectively. Maternal platelet activation (P-selectin positive platelets) was linked with disease severity (sFlt-1/placental growth factor) and maternal plasma IL-1β and sVCAM-1 only in late-onset preeclampsia. A statistically significant correlation with αIIbβ3 expressing platelets and sFlt-1, IL-1β, and sVCAM-1 was not observed.
Conclusions:
These findings identify that thrombo-inflammation is regulated in L-PE and E-PE through likely disjunct mechanisms supporting a role of maternal factors (eg, maternal platelet activation) involved in L-PE. Further studies with a larger cohort of patients are required to fully elucidate the mechanistic relevance of these findings.
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