Author(s): Mestre L, Docagne F, Correa F, Lora F, Hernangmez M, , Mestre L, Docagne F, Correa F, Lora F, Hernangmez M,
Abstract Share this page
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.
This article was published in Mol Cell Neurosci
and referenced in Journal of Multiple Sclerosis
- Sergey Suchkov
Translational toolsas applicable to autoimmune disorders: antibody-proteases as a generation of highly informative and unique biomarkersto monitor subclinical and clinical stages of demyelination in multiple sclerosis (MS)
PPT Version | PDF Version