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Updated: Jun 8, 2026

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Cannabinoid receptor type 2 (CB2) deficiency alters atherosclerotic lesion formation in hyperlipidemic Ldlr-null mice

Courtney D Netherland1, Theresa G Pickle, Alicia Bales

  • 1Department of Biochemistry and Molecular Biology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614-0581, USA.

Atherosclerosis
|September 18, 2010
PubMed
Abstract

Insights

Cannabinoid receptor 2 (CB2) gene deletion in mice with hyperlipidemia increased atherosclerotic plaque macrophage and smooth muscle cell content. This suggests CB2 receptor manipulation may have complex effects on atherosclerosis development and plaque stability.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pharmacology

Background:

  • Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.
  • The role of cannabinoid receptor 2 (CB2) in atherogenesis remains incompletely understood.
  • Low density lipoprotein receptor-deficient (Ldlr(-/-)) mice are a standard model for studying atherosclerosis.

Purpose of the Study:

  • To investigate the role of CB2 in hyperlipidemia-induced atherosclerosis.
  • To determine the effects of systemic CB2 gene deletion on atherogenesis in Ldlr(-/-) mice.

Main Methods:

  • Ldlr(-/-) and CB2/Ldlr double knockout (CB2(-/-)Ldlr(-/-)) mice were fed an atherogenic diet for 8 and 12 weeks.
  • Atherosclerotic lesion area, macrophage and smooth muscle cell (SMC) content, lesional apoptosis, and extracellular matrix components were analyzed.
  • Matrix metalloproteinase 9 (MMP) levels and activity were assessed in vitro and in vivo.

Main Results:

  • No significant difference in lesion area was observed between groups at 8 or 12 weeks.
  • After 12 weeks, CB2(-/-)Ldlr(-/-) lesions showed increased macrophage and SMC content.
  • Lesional apoptosis was reduced, collagen content decreased, elastin fragmented, and MMP9 levels increased in CB2(-/-)Ldlr(-/-) mice after 12 weeks.
  • In vitro, CB2(-/-) macrophages exhibited higher MMP9 activity.

Conclusions:

  • CB2 receptor deficiency exacerbates atherogenesis in Ldlr-null mice.
  • CB2 deficiency increases plaque macrophage and SMC content, reduces apoptosis, and alters extracellular matrix composition.
  • Upregulation of MMP9 contributes to these changes, suggesting complex roles for CB2 in atherosclerosis and plaque stability.

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