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

Neurology

Journal of Multiple Sclerosis

Author(s): Mestre L, Docagne F, Correa F, Lora F, Hernangmez M, , Mestre L, Docagne F, Correa F, Lora F, Hernangmez M,

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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

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    Translational tools as applicable to autoimmune disorders: antibody-proteases as a generation of highly informative and unique biomarkers to monitor subclinical and clinical stages of demyelination in multiple sclerosis (MS)
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