A cannabinoid agonist interferes with the progression of a chronic model of multiple sclerosis by downregulating adhesion molecules

Mol Cell Neurosci. 2009 Feb;40(2):258-66. doi: 10.1016/j.mcn.2008.10.015. Epub 2008 Nov 19.

Abstract

Adhesion molecules are critical players in the regulation of transmigration of blood leukocytes across the blood-brain barrier in multiple sclerosis (MS). Cannabinoids (CBs) are potential therapeutic agents in the treatment of MS, but the mechanisms involved are only partially known. Using a viral model of MS we observed that the cannabinoid agonist WIN55,212-2 administered at the time of virus infection suppresses intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in brain endothelium, together with a reduction in perivascular CD4+ T lymphocytes infiltrates and microglial responses. WIN55,212-2 also interferes with later progression of the disease by reducing symptomatology and neuroinflammation. In vitro data from brain endothelial cell cultures, provide the first evidence of a role of peroxisome proliferator-activated receptors gamma (PPARgamma) in WIN55,212-2-induced downregulation of VCAM-1. This study highlights that inhibition of brain adhesion molecules by WIN55,212-2 might underline its therapeutic effects in MS models by targeting PPAR-gamma receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal / physiology
  • Benzoxazines / pharmacology
  • Calcium Channel Blockers / pharmacology
  • Cannabinoids / agonists*
  • Cannabinoids / pharmacology*
  • Cannabinoids / therapeutic use
  • Cardiovirus Infections / physiopathology
  • Disease Models, Animal
  • Disease Progression
  • Endothelium / cytology
  • Endothelium / drug effects*
  • Endothelium / metabolism
  • Female
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Mice
  • Morpholines / pharmacology
  • Motor Activity / physiology
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / pathology*
  • Multiple Sclerosis / physiopathology
  • Naphthalenes / pharmacology
  • PPAR gamma / metabolism
  • Receptor, Cannabinoid, CB1 / metabolism
  • Receptor, Cannabinoid, CB2 / metabolism
  • Theilovirus / metabolism
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism*

Substances

  • Benzoxazines
  • Calcium Channel Blockers
  • Cannabinoids
  • Morpholines
  • Naphthalenes
  • PPAR gamma
  • Receptor, Cannabinoid, CB1
  • Receptor, Cannabinoid, CB2
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • (3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone