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Collagen-linked fluorescence in human atherosclerotic plaques
W K Lee1, J Bell, E Kilpatrick
1Department of Pathological Biochemistry, Western Infirmary, Glasgow, Scotland, UK.
Atherosclerosis
|January 25, 1993
Summary
Advanced glycosylation endproducts (AGEs) in collagen change within arteries during atherosclerosis. Collagen-linked fluorescence (CLF) decreased in plaque-covered aorta, suggesting localized AGE-collagen modifications impact disease.
Area of Science:
- Biochemistry
- Cardiovascular Research
- Pathology
Background:
- Advanced glycosylation endproducts (AGEs) are crosslinks formed during the Maillard reaction.
- The presence and localization of AGE-modified collagen within arteries, particularly in atherosclerosis, remain largely uncharacterized.
Purpose of the Study:
- To investigate local changes in AGE-modified collagen within human arterial tissue and atherosclerotic plaques.
- To determine the relationship between collagen-linked fluorescence (CLF) and the presence/severity of atherosclerosis.
Main Methods:
- Quantification of AGE-modified collagen using collagen-linked fluorescence (CLF) in human aorta, coronary arteries, tendon, skin, and atherosclerotic plaques.
- Comparison of CLF levels in atheroma-free arterial segments versus plaque-covered areas.
- Correlation analysis between CLF in different tissues and plaque severity.
Main Results:
- All tissues exhibited a characteristic fluorescence peak, indicating AGE-modified collagen.
- CLF in the aorta was significantly decreased in areas covered by superficial plaque compared to adjacent atheroma-free segments (P = 0.01).
- Lower CLF was observed in superficial atherosclerotic plaques of individuals with low to moderate atheroma compared to those with severe atheroma (P = 0.0466).
Conclusions:
- Local alterations in vascular AGE-collagen concentration occur during atherosclerosis.
- These findings suggest a potential pathogenetic role for localized AGE-collagen modifications in the development and progression of atherosclerosis.