Evidence that macrophages in atherosclerotic lesions contain angiotensin II

D D Potter1, C G Sobey, P K Tompkins

  • 1Department of Internal Medicine, Cardiovascular Center and Center on Aging, University of Iowa College of Medicine, Iowa City 52242, USA.

Circulation
|September 4, 1998
PubMed
Abstract

Insights

Angiotensin II (Ang II) is present in atherosclerotic lesions in both monkeys and humans. This peptide colocalizes with macrophages and decreases as atherosclerosis regresses in monkeys.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Cell Biology

Background:

  • Human mononuclear leukocytes possess significant levels of angiotensin II (Ang II).
  • Previous research indicates Ang II presence in leukocytes.
  • The study investigates Ang II localization within monocyte/macrophages in atherosclerotic lesions.

Purpose of the Study:

  • To determine if Ang II is present in monocyte/macrophages within atherosclerotic lesions.
  • To investigate the colocalization of Ang II and macrophages in atherosclerotic vessels.
  • To assess changes in Ang II levels during atherosclerosis regression.

Main Methods:

  • Analysis of thoracic aorta and coronary artery segments from normal, atherosclerotic, and regression groups of cynomolgus monkeys.
  • Examination of human coronary arterial atherosclerotic lesions obtained via directional atherectomy.
  • Immunohistochemical staining for Ang II using specific antisera and macrophage markers.

Main Results:

  • Atherosclerotic lesions in monkeys and humans showed positive staining for Ang II.
  • Ang II staining colocalized with macrophages in the intima-media of atherosclerotic monkey vessels.
  • Ang II and macrophage staining decreased in monkey lesions after atherosclerosis regression.

Conclusions:

  • Angiotensin II is confirmed to be present in atherosclerotic lesions in both primate models and humans.
  • Findings suggest a role for Ang II in atherosclerotic plaque development, particularly in association with macrophages.
  • The study demonstrates a reduction in Ang II within lesions during the regression phase of atherosclerosis in monkeys.

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