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Published on: April 13, 2018
S100 calcium-binding protein A8 exacerbates deep vein thrombosis in vascular endothelial cells
Junyu Chi1, Qitao Wang1, Zhen Wang1
1Vascular Gland Surgery, The First Affiliated Hospital of Hebei North University, Zhangjiakou, 075000, Hebei, China.
Insights
S100A8 protein is linked to deep vein thrombosis (DVT) development. This protein may worsen DVT by increasing inflammation and thrombus formation via the NLRP3/Caspase-1/IL-1β pathway.
Area of Science:
- Biomedical research
- Vascular biology
- Thrombosis research
Background:
- Inflammation and vascular endothelial damage are key factors in deep vein thrombosis (DVT) development.
- The S100 calcium-binding protein A8 (S100A8) has been implicated in these processes.
Purpose of the Study:
- To investigate the association between S100A8 and DVT.
- To elucidate the role of S100A8 in the pathogenesis of DVT.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure S100A8 and interleukin-1 beta (IL-1β) levels in blood samples from DVT patients and controls.
- Human umbilical vein endothelial cells were activated with recombinant S100A8.
- A rat model of DVT was established.
Main Results:
- Elevated S100A8 and IL-1β levels were observed in DVT patients compared to controls.
- S100A8 activation of endothelial cells promoted inflammatory responses.
- Infiltration of S100A8 was found to sustain local inflammation and thrombus formation in the DVT model.
Conclusions:
- S100A8 plays a significant role in DVT development.
- S100A8 may exacerbate DVT by amplifying the NLRP3/Caspase-1/IL-1β signaling pathway in vascular endothelial cells, contributing to inflammation and thrombosis.
Abstract:
Previous studies highlighting the pivotal function of the S100A8 protein have shown that inflammation and vascular endothelial harm play a major role in deep vein thrombosis (DVT) development, as evidenced by earlier studies highlighting the pivotal function of the S100 calcium-binding protein A8 (S100A8). Therefore, we aimed to establish a connection between S100A8 and DVT and investigate the role of S100A8 in DVT development. Blood specimens were taken from 23 patients with DVT and 31 controls. The fluctuation and association for S100A8 and interleukin-1 beta (IL-1β) in the specimens was assessed using enzyme-linked immunosorbent assay. We also used the human recombinant protein S100A8 to activate human umbilical vein endothelial cells and created a rat model to explore the possible relationship between them. Studies have shown that the infiltration of S100A8 sustains local inflammation and thrombus formation, which may exacerbate DVT by amplifying NLRP3/Caspase-1/IL-1β signals in the vascular endothelial cells.
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