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Structural and functional modifications of human aorta proteoglycans in atherosclerosis
G M Cherchi1, R Coinu, P Demuro
1Institute of Applied Biology, University of Sassari, Italy.
Matrix (Stuttgart, Germany)
|December 1, 1990
Summary
Atherosclerotic plaques show altered proteoglycan (PG) composition and increased low-density lipoprotein (LDL) interactions compared to normal aorta. These changes in glycosaminoglycans (GAGs) may contribute to atherosclerosis development.
Area of Science:
- Biochemistry
- Cardiovascular Research
- Atherosclerosis Pathogenesis
Background:
- Proteoglycans (PGs) are crucial components of the extracellular matrix in blood vessels.
- Alterations in PG composition are implicated in the development of atherosclerosis.
Purpose of the Study:
- To investigate the differences in proteoglycan composition and low-density lipoprotein (LDL) interactions between normal and atherosclerotic human aorta.
- To understand the role of PGs and glycosaminoglycans (GAGs) in the pathogenesis of atherosclerosis.
Main Methods:
- Sequential extraction of PGs using varying guanidine hydrochloride (GuHCl) concentrations.
- Electrophoretic glycosaminoglycan (GAG) analysis.
- Gel-chromatography and CsCl density gradient centrifugation for PG characterization.
- Affinity chromatography to study LDL/PG and LDL/GAG interactions.
Main Results:
- Atherosclerotic aorta samples had lower hexuronic acid content and higher chondroitinase AC resistant material compared to normal samples.
- PGs from atherosclerotic areas showed a higher proportion of dermatan sulphate (DS) and reduced content of high hydrodynamic size PGs.
- Glycosaminoglycans (GAGs) from atherosclerotic PGs exhibited stronger interaction with human LDL, indicating increased LDL binding affinity.
Conclusions:
- Atherosclerosis is associated with significant changes in aortic proteoglycan composition, including altered GAG profiles and reduced PG size.
- Increased affinity of atherosclerotic PGs and GAGs for LDL suggests a potential mechanism contributing to LDL accumulation in atherosclerotic lesions.