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Updated: Oct 1, 2026
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
Changes in the phospholipid composition of the arterial cell can result in severe atherosclerotic lesions
F A. Kummerow1, L S. Cook, E Wasowicz
1The Burnsides Research Laboratory, University of Illinois, 61801, Urbana, IL, USA
Insights
Elevated oxysterol levels in patients with coronary artery bypass grafting (CABG) correlate with increased calcium influx into endothelial cells. This suggests oxysterols may contribute to atherosclerosis by altering arterial cell membranes and promoting calcification.
Area of Science:
- Cardiovascular Biology
- Atherosclerosis Research
- Cellular Physiology
Background:
- Oxysterols are cholesterol oxidation products implicated in cardiovascular disease.
- Atherosclerosis is characterized by arterial wall thickening and calcification.
- Endothelial cell function is critical in maintaining vascular health.
Purpose of the Study:
- To investigate the relationship between plasma oxysterol concentrations and vascular tissue composition in patients undergoing coronary artery bypass grafting (CABG).
- To determine the effect of oxysterols on calcium influx into human endothelial cells.
- To explore the role of sphingomyelin in oxysterol-induced vascular changes.
Main Methods:
- Comparison of plasma oxysterol levels and vascular phospholipid composition between CABG patients and controls.
- In vitro culture of human endothelial cells with plasma from CABG patients and controls, with and without added oxysterols.
- Measurement of calcium (45Ca2+) influx into endothelial cells.
- Phospholipid analysis of arterial and saphenous vein tissues.
Main Results:
- CABG patients exhibited higher plasma oxysterol concentrations compared to controls.
- Endothelial cells cultured in plasma with elevated oxysterols showed significantly increased calcium influx.
- Arterial tissue from CABG patients had a higher sphingomyelin content (48.2%) than saphenous vein (24%) or umbilical cord arteries (10%).
- Saphenous veins, with lower sphingomyelin, lacked atherosclerotic lesions.
Conclusions:
- Oxysterols increase calcium influx into endothelial cells, potentially contributing to vascular calcification in atherosclerosis.
- Elevated sphingomyelin in arterial cell membranes may be linked to oxysterol-induced calcium influx and lesion development.
- These findings highlight a potential mechanism by which oxysterols promote the progression of atherosclerosis.
Abstract:
The oxysterol concentration in the plasma and the phospholipid composition of vascular tissue obtained by coronary artery bypass grafting (CABG) were compared with plasma and vascular tissue from age and sex matched controls. The plasma from CABG patients had a higher concentration of oxysterols than was present in the controls. Human endothelial cells were cultured for 72 hours in a medium containing plasma obtained from CABG patients, from controls or from the same controls to which 5 oxysterols were added to make the total oxysterol level equivalent to that in the CABG plasma and then pulsed with calcium (45Ca(2+)) for one hr. A significantly higher influx of 45Ca(2+) was noted in the endothelial cells cultured in the plasma obtained from CABG patients and from the controls with 5 added oxysterols, but not in those cultured without added oxysterols indicating that oxysterols increased calcium influx into endothelial cells. A phospholipid analysis indicated that the arterial tissue from CABG patients had 48.2% sphingomyelin in its phospholipid fraction compared to 10% in arterial tissue from umbilical cords. The saphenous vein obtained during CABG surgery from the same patient had only 24% sphingomyelin in its phospholipid fraction and unlike the coronary arteries had no atherosclerotic lesions. The higher level of oxysterol in the plasma of patients suffering from severe atherosclerosis could increase the concentration of sphingomyelin in the arterial cell membrane and thereby increase calcium influx required for producing the calcific type VII lesions in the coronary arteries.
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