Low-Density Lipoprotein Induces Vascular Adhesion Molecule Expression on Human Endothelial Cells

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 511-516 ◽  
Author(s):  
Hermann Haller ◽  
Doris Schaper ◽  
Wolfgang Ziegler ◽  
Sebastian Philipp ◽  
Martin Kuhlmann ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Adhesion Molecule Expression ◽  
Human Endothelial Cells ◽  
Vascular Adhesion

Abstract 395: Lipoprotein Apheresis of Hypercholesterolemic Patients Mediates Vasoprotective Gene Expression in Human Endothelial Cells

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Henning Morawietz ◽  
Winfried Goettsch ◽  
Melanie Brux ◽  
Manja Reimann ◽  
Stefan R Bornstein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Molecular Mechanisms ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Human Endothelial Cells ◽  
Lipoprotein Apheresis

OBJECTIVE Hypercholesterolemia is an important risk factor of cardiovascular diseases. Lipoprotein apheresis is an efficient strategy to reduce the serum low-density lipoprotein (LDL)-cholesterol and lipoprotein(a) levels and cardiovascular complications in patients with severe hypercholesterolemia. The underlying molecular mechanisms are not well-understood. In this study, we analyzed the impact of lipoprotein apheresis on gene expression in human endothelial cells. METHODS Human endothelial cells were stimulated with serum of hypercholesterolemic patients before and after lipoprotein apheresis. The expression of endothelial lipoprotein receptors, nitric oxide (NO) synthase and adhesion molecules was quantified by real-time PCR and Western blot. RESULTS Lipoprotein apheresis reduced the expression of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in endothelial cells. Low-density lipoprotein (LDL) receptor expression remained unchanged. The mRNA expression of the endothelial nitric oxide synthase (eNOS) was increased with serum of hypercholesterolemic patients after lipoprotein apheresis. In contrast, endothelial expression of vascular cell adhesion molecule 1 (VCAM-1) was reduced in response to serum after lipoprotein apheresis. CONCLUSION Lipoprotein apheresis reduced the expression of the proatherosclerotic oxLDL receptor LOX-1 and adhesion molecule VCAM-1 and increased the expression of vasoprotective and NO generating eNOS in human endothelial cells in response to serum of hypercholesterolemic patients. These novel molecular mechanisms may account for the antiatherosclerotic and vasoprotective potential of lipoprotein apheresis in patients with hypercholesterolemia.

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