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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Cannabinoid receptor 2 signaling does not modulate atherogenesis in mice

Florian Willecke1, Katharina Zeschky, Alexandra Ortiz Rodriguez

  • 1Department of Cardiology, University of Freiburg, Freiburg, Germany.

Plos One
|May 5, 2011
PubMed
Abstract

Insights

Cannabinoid receptor 2 (CB2) activation or deletion does not significantly impact atherosclerosis development in mice. These findings suggest CB2 is not a viable therapeutic target for reducing atherosclerotic plaque.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Cannabinoid receptor 2 (CB2) is implicated in inflammation and atherosclerosis.
  • Direct evidence linking CB2 to atherosclerotic lesion formation is limited.
  • This study investigates the role of CB2 in murine atherogenesis.

Purpose of the Study:

  • To characterize the role of the CB2 receptor in the development of atherosclerosis in mice.
  • To determine if CB2 activation or deficiency affects atherosclerotic plaque formation and composition.

Main Methods:

  • Low density lipoprotein receptor-deficient (LDLR(-/-)) mice were fed a high-cholesterol diet.
  • Mice received intraperitoneal injections of a selective CB2 agonist (JWH-133) or vehicle.
  • Atherogenesis was assessed by analyzing aortic root and arch lesions, plaque content, and inflammatory markers.

Main Results:

  • CB2 activation with JWH-133 did not alter intimal lesion size in LDLR(-/-) mice.
  • Genetic deficiency of CB2 in CB2(-/-)/LDLR(-/-) mice also did not affect lesion size.
  • Neither pharmacologic activation nor genetic deletion of CB2 modulated inflammatory cytokine expression or inflammatory cell adhesion.

Conclusions:

  • Both activation and deletion of CB2 do not significantly modulate atherogenesis in mice.
  • While CB2 is involved in other inflammatory processes, it does not appear to be a suitable therapeutic target for atherosclerosis.
  • Further research may be needed to clarify the precise role of CB2 in cardiovascular inflammation.

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