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Complement receptors in atherosclerotic lesions.

E Saito¹, T Fujioka, H Kanno

¹2nd Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.

Artery

|January 1, 1992

Summary

This study investigated complement receptors in atherosclerotic lesions. Macrophage complement receptors are expressed during complement activation, suggesting a role in low-density lipoprotein (LDL) uptake by macrophages in atherosclerosis.

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Area of Science:

Cardiovascular Biology
Immunology
Pathology

Background:

Cholesterol accumulation in arteries is key to atherosclerosis.
Oxidized low-density lipoprotein (LDL) is implicated in atherogenesis.
The mechanism of lipid accumulation in macrophages remains unclear.

Purpose of the Study:

To investigate the presence and role of complement receptors in human atherosclerotic lesions.
To explore the relationship between the complement system and macrophage lipid uptake in atherosclerosis.

Main Methods:

Analysis of autopsy-obtained aortic sections from patients with varying degrees of arterial thickening.
Detection of C3b receptors using sheep erythrocytes bearing human C3b (EAC1423b cells).
Immunostaining for apolipoprotein B (apo B), C5b-9 complex, macrophages, complement receptor 1 (CR1), and complement receptor 3 (CR3).

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Main Results:

C3b receptors adhered specifically to aortic sections with intimal thickening, not intact arteries.
Complement receptor-expressing cells in thickened intima and atheroma were identified as macrophages.
Apo B was found extracellularly, and C5b-9 complex was present in the intima and media of affected arteries.
Macrophage complement receptors were expressed in atherosclerotic lesions during complement system activation.

Conclusions:

The complement system is activated in atherosclerotic lesions.
Macrophage complement receptors (CR1 and CR3) are expressed in atherosclerotic lesions.
These findings suggest the complement system and its receptors may mediate LDL uptake by macrophages, contributing to atherogenesis.