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Evidence that glucose increases monocyte binding to human aortic endothelial cells

J A Kim¹, J A Berliner, R D Natarajan

¹Department of Diabetes, Endocrinology, and Metabolism, City of Hope Medical Center, Duarte, California 91010.

|September 1, 1994

Summary

High glucose levels significantly increase monocyte adhesion to endothelial cells, a key step in atherosclerosis development. This effect is chronic, not acute, and mediated by beta-2 integrins, not major adhesion molecules.

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Area of Science:

Cardiovascular Biology
Endocrinology
Immunology

Background:

Diabetes mellitus accelerates atherosclerosis.
Monocyte adhesion to vascular endothelium is critical in atherosclerosis.
The impact of glucose on monocyte binding remains unclear.

Purpose of the Study:

To investigate the effect of chronic high glucose exposure on human monocyte binding to human aortic endothelial cells (HAEC).

Main Methods:

HAEC were cultured in high glucose (25 mM) or normal glucose (5.5 mM) for 7-10 days.
Monocyte binding assays were performed.
Mannitol was used to assess hyperosmolar effects.
Antibodies against adhesion molecules (E-selectin, VCAM-1, ICAM-1, beta-2 integrin, VLA-4) were utilized.

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Main Results:

Chronic high glucose significantly increased monocyte binding to HAEC (188 cells/field vs. 111 cells/field).
Mannitol and acute glucose exposure did not affect binding.
High glucose did not induce E-selectin, VCAM-1, or ICAM-1.
Anti-beta-2 integrin antibody reduced binding, while anti-VLA-4 antibody did not.

Conclusions:

Chronic hyperglycemia, not hyperosmolarity or acute exposure, enhances monocyte adhesion to the endothelium.
This increased binding is mediated via beta-2 integrins, independent of major adhesion molecules like ICAM-1.
These findings suggest a mechanism by which hyperglycemia contributes to accelerated atherosclerosis in diabetes.