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Angiotensin II increases monocyte binding to endothelial cells
J A Kim1, J A Berliner, J L Nadler
1Department of Diabetes & Endocrinology, City of Hope Medical Center, Duarte, CA 91010, USA.
Biochemical and Biophysical Research Communications
|September 24, 1996
Summary
Angiotensin II (AII) accelerates atherosclerosis by increasing monocyte adhesion to endothelial cells. This effect was observed in human and rabbit aortic cells and was blocked by AII receptor inhibitors.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Biology
- Atherosclerosis Research
Background:
- Angiotensin II (AII) is implicated in hypertension and atherosclerosis pathogenesis.
- Monocyte adhesion to endothelium is an early event in atherosclerosis.
- The specific impact of AII on monocyte binding requires further investigation.
Purpose of the Study:
- To investigate the effect of Angiotensin II (AII) on monocyte binding to endothelial cells.
- To determine the role of AII receptors in this process.
- To explore the molecular mechanisms underlying AII-induced monocyte adhesion.
Main Methods:
- Treatment of human aortic endothelial cells (HAEC) and rabbit aortic cells (RAEC) with AII.
- Assessment of monocyte and neutrophil adhesion.
- Evaluation of E-selectin, VCAM-1, and ICAM-1 expression.
- Use of AII receptor inhibitors (Type I and Type II).
Main Results:
- AII treatment significantly induced monocyte adhesion to HAEC and RAEC.
- Neutrophil adhesion was not affected by AII.
- AII-induced monocyte binding was reduced by AII receptor inhibitors.
- No induction of E-selectin, VCAM-1, or ICAM-1 was observed.
Conclusions:
- Angiotensin II promotes monocyte binding to the endothelium.
- This effect is mediated through AII receptors.
- AII may accelerate atherosclerosis by enhancing monocyte endothelial interactions.