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Updated: May 14, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Lipoprotein apheresis of hypercholesterolemic patients mediates vasoprotective gene expression in human endothelial
Henning Morawietz1, Winfried Goettsch, Melanie Brux
1Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University Clinical Center, University Hospital Carl Gustav Carus, Dresden University of Technology, Fetscherstr 74, 01307 Dresden, Germany. Henning.Morawietz@tu-dresden.de
Insights
Lipoprotein apheresis reduces harmful LOX-1 and VCAM-1 expression while increasing beneficial eNOS in endothelial cells. These molecular changes in hypercholesterolemia patients may explain its antiatherosclerotic effects.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Endothelial Cell Biology
Background:
- Hypercholesterolemia is a major risk factor for cardiovascular diseases.
- Lipoprotein apheresis effectively lowers low-density lipoprotein (LDL)-cholesterol and lipoprotein(a), reducing cardiovascular complications in severe hypercholesterolemia.
- The precise molecular mechanisms of lipoprotein apheresis remain incompletely understood.
Purpose of the Study:
- To investigate the impact of lipoprotein apheresis on gene expression in human endothelial cells.
- To elucidate the molecular pathways underlying the vasoprotective effects of lipoprotein apheresis.
Main Methods:
- Human endothelial cells were treated with serum from hypercholesterolemic patients before and after lipoprotein apheresis.
- Quantitative analysis of endothelial lipoprotein receptors, nitric oxide (NO) synthase, and adhesion molecules was performed using real-time PCR and Western blot.
Main Results:
- Lipoprotein apheresis significantly decreased the expression of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in endothelial cells.
- Endothelial nitric oxide synthase (eNOS) mRNA expression increased following apheresis.
- Expression of vascular cell adhesion molecule 1 (VCAM-1) was reduced post-apheresis.
Conclusions:
- Lipoprotein apheresis downregulates proatherosclerotic factors LOX-1 and VCAM-1 while upregulating the vasoprotective, NO-producing eNOS in endothelial cells.
- These molecular alterations provide novel insights into the antiatherosclerotic and vasoprotective benefits of lipoprotein apheresis in hypercholesterolemia management.
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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