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Updated: May 21, 2026

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
Published on: September 15, 2017
Endothelial cells obtained from patients affected by chronic venous disease exhibit a pro-inflammatory phenotype
Veronica Tisato1, Giorgio Zauli, Rebecca Voltan
1Department of Morphology and Embryology and LTTA Centre, University of Ferrara, Ferrara, Italy.
Insights
Chronic venous disease (CVD) involves pro-inflammatory vein endothelial cells (VECs). These VECs show increased inflammatory markers and cytokine release, contributing to systemic inflammation in CVD patients.
Area of Science:
- Vascular Biology
- Immunology
- Cell Biology
Background:
- The inflammatory characteristics of vein endothelium in chronic venous disease (CVD) are not well understood.
- Investigating large vein endothelium offers new insights into large vessel physiopathology.
Purpose of the Study:
- To characterize the phenotype and function of venous endothelial cells (VECs) from patients with CVD.
- To compare VECs from CVD patients with those from healthy controls.
Main Methods:
- VEC cultures were established from surgical vein specimens of CVD patients and controls.
- Flow cytometry was used to assess surface marker expression (CD31/PECAM-1, CD146, ICAM-1).
- Cell proliferation, starvation resistance, migration, and cytokine release (OPG, VEGF) were evaluated. NF-kB activity was assessed.
Main Results:
- Pathological VECs from CVD patients showed increased expression of CD31/PECAM-1, CD146, and ICAM-1 compared to controls.
- VECs from more advanced CVD cases exhibited stronger pro-inflammatory marker expression.
- Pathological VECs displayed higher proliferation and starvation resistance but lower migratory capacity.
- Elevated NF-kB activity led to increased release of osteoprotegerin (OPG) and vascular endothelial growth factor (VEGF) in pathological VECs.
- CVD patients had higher serum OPG and VEGF levels than healthy controls.
Conclusions:
- Vein endothelial cells from CVD patients exhibit a pro-inflammatory phenotype.
- This pro-inflammatory phenotype of VECs may significantly contribute to systemic inflammation in CVD.
- These findings highlight VECs as potential targets for managing CVD-related inflammation.
Background:
The inflammatory properties of vein endothelium in relation to chronic venous disease (CVD) have been poorly investigated. Therefore, new insights on the characteristics of large vein endothelium would increase our knowledge of large vessel physiopathology.
Methodology/Principal Findings:
Surgical specimens of veins were obtained from the tertiary venous network (R3) and/or saphenous vein (SF) of patients affected by CVD and from control individuals. Highly purified venous endothelial cell (VEC) cultures obtained from CVD patients were characterized for morphological, phenotypic and functional properties compared to control VEC. An increase of CD31/PECAM-1, CD146 and ICAM-1 surface levels was documented at flow cytometry in pathological VEC with respect to normal controls. Of note, the strongest expression of these pro-inflammatory markers was observed in VEC obtained from patients with more advanced disease. Similarly, spontaneous cell proliferation and resistance to starvation was higher in pathological than in normal VEC, while the migratory response of VEC showed an opposite trend, being significantly lower in VEC obtained from pathological specimens. In addition, in keeping with a higher baseline transcriptional activity of NF-kB, the release of the pro-inflammatory cytokines osteoprotegerin (OPG) and vascular endothelial growth factor (VEGF) was higher in pathological VEC cultures with respect to control VEC. Interestingly, there was a systemic correlation to these in vitro data, as demonstrated by higher serum OPG and VEGF levels in CVD patients with respect to normal healthy controls.
Conclusion/Significance:
Taken together, these data indicate that large vein endothelial cells obtained from CVD patients exhibit a pro-inflammatory phenotype, which might significantly contribute to systemic inflammation in CVD patients.
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