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.

Plos One
|June 28, 2012
PubMed

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.
Abstract

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