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Plasma cholesterol regulates soluble cell adhesion molecule expression in familial hypercholesterolemia
T Sampietro1, M Tuoni, M Ferdeghini
1CNR Institute of Clinical Physiology and S. Chiara Hospital, University of Pisa, Italy.
Circulation
|October 7, 1997
Summary
High cholesterol contributes to endothelial dysfunction. LDL apheresis in familial hypercholesterolemia patients significantly reduced soluble adhesion molecules, suggesting cholesterol directly influences endothelial adhesiveness.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Immunology
Background:
- Hypercholesterolemia is linked to endothelial dysfunction.
- High plasma cholesterol may upregulate endothelial adhesiveness.
- This phenomenon might be reversible.
Purpose of the Study:
- Investigate soluble endothelial leukocyte adhesion molecules (sELAMs) in familial hypercholesterolemia patients.
- Determine if high cholesterol directly upregulates endothelial adhesiveness.
- Assess the reversibility of this upregulation via LDL apheresis.
Main Methods:
- Selective LDL apheresis using dextran sulfate columns on patients with familial hypercholesterolemia.
- Measurement of soluble intercellular adhesion molecule-1 (sICAM-1) and sELAM-1 before and after LDL apheresis.
- Exclusion of removal by extracorporeal circulation components.
Main Results:
- LDL apheresis significantly reduced total cholesterol (74%), LDL cholesterol (82%), and sICAM-1/sELAM-1 levels (P<.0001, P<.0004).
- Basal sICAM-1 and sELAM-1 levels were elevated compared to controls and decreased post-apheresis.
- Pre- and post-treatment sICAM-1/sELAM-1 levels correlated positively with total cholesterol (P<.0001, P<.001).
Conclusions:
- Results confirm upregulation of endothelial adhesiveness in clinical hypercholesterolemia.
- Suggest a direct role for cholesterol in regulating endothelial adhesiveness.
- Findings support cholesterol's direct role in familial hypercholesterolemia, independent of other inflammatory markers.