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Human pulmonary valve endothelial cells express functional adhesion molecules for leukocytes
Evan L Dvorin1, Joel Jacobson, Stephen J Roth
1Department of Surgery, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA.
The Journal of Heart Valve Disease
|October 21, 2003
Summary
Human pulmonary valve endothelial cells (HPVEC) express functional leukocyte adhesion molecules, suggesting they can initiate inflammatory cell adhesion. Hemodynamic forces may protect cardiac valves from inflammation in vivo.
Area of Science:
- Immunology
- Cardiovascular Biology
- Endothelial Cell Biology
Background:
- Cardiac valve endothelium appears protected from inflammatory cell infiltration in heart transplant rejection.
- The role of valve endothelium's inherent properties in this protection is unclear.
Purpose of the Study:
- To investigate leukocyte adhesion molecule expression and function in human pulmonary valve endothelial cells (HPVEC).
- To determine if valve endothelium is inherently capable of initiating leukocyte adhesion.
Main Methods:
- Cultured HPVEC were stimulated with tumor necrosis factor-alpha (TNF-alpha).
- Expression of E-selectin, ICAM-1, and VCAM-1 was analyzed.
- Static cell adhesion assays were performed using HL-60 and U937 cell lines.
Main Results:
- HPVEC expressed E-selectin, ICAM-1, and VCAM-1 upon TNF-alpha stimulation.
- E-selectin mediated adhesion of HL-60 and U937 cells after 5 hours of TNF-alpha treatment.
- VCAM-1 primarily mediated U937 cell adhesion after 24 hours of TNF-alpha treatment.
Conclusions:
- Human pulmonary valve endothelial cells express functional leukocyte adhesion molecules in vitro.
- Cardiac valve endothelium is capable of initiating leukocyte adhesion.
- Hemodynamic forces, not just endothelial properties, may contribute to valve protection from inflammation in vivo.