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Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Lack of neutrophil-derived CRAMP reduces atherosclerosis in mice

Yvonne Döring1, Maik Drechsler, Sarawuth Wantha

  • 1Institute for Cardiovascular Prevention, Ludwig-Maximilians University München, Munich, Germany.

Circulation Research
|March 8, 2012
PubMed

Insights

Neutrophil cathelicidins promote atherosclerosis by increasing inflammatory monocyte recruitment. Reducing cathelicidin levels in neutrophils lessens atherosclerotic lesion size and macrophage accumulation.

Area of Science:

  • Immunology
  • Cardiovascular Research

Background:

  • Neutrophils are implicated in early atherosclerosis development.
  • The precise mechanisms of neutrophil-driven atherosclerosis are not fully understood.

Purpose of the Study:

  • To investigate the role of the neutrophil granule protein cathelicidin (CRAMP in mice, LL37 in humans) in atherosclerosis progression.

Main Methods:

  • Comparative analysis of Apoe(-/-) and Cramp(-/-) Apoe(-/-) mice.
  • Detection of CRAMP in atherosclerotic aortas using immunohistochemistry.
  • Intravital microscopy to observe CRAMP deposition and monocyte adhesion.
  • Assessment of formyl-peptide receptor dependency.

Main Results:

  • Cramp(-/-) Apoe(-/-) mice showed reduced atherosclerotic lesion sizes and fewer macrophages compared to controls.
  • CRAMP was localized to neutrophils, not monocytes or macrophages, in atherosclerotic aortas.
  • Activated neutrophils deposited CRAMP on inflamed endothelium, promoting classical monocyte and neutrophil adhesion via formyl-peptide receptor signaling.

Conclusions:

  • Cathelicidins enhance atherosclerosis by promoting the recruitment of inflammatory monocytes.
  • Targeting cathelicidin may offer a therapeutic strategy for atherosclerosis.
Abstract

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