A role for Apolipoprotein A-I in the pathogenesis of multiple sclerosis
| Autor: | Joshua N. Douglas, Lidia A. Gardner, Chassidy J. Groover, David D. Brand, Sangmin Lee, Lindsay Meyers, Michael C. Levin |
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| Rok vydání: | 2014 |
| Předmět: |
Adult
Male Encephalomyelitis Autoimmune Experimental Multiple Sclerosis Apolipoprotein B Encephalomyelitis Immunology Freund's Adjuvant Mice Transgenic Biology Pathogenesis Mice Western blot medicine Immunology and Allergy Animals Humans Electrophoresis Gel Two-Dimensional medicine.diagnostic_test Apolipoprotein A-I Multiple sclerosis Neurodegeneration medicine.disease Fluoresceins Peptide Fragments Mice Inbred C57BL Disease Models Animal Neurology Gene Expression Regulation Case-Control Studies biology.protein Cytokines Evoked Potentials Visual lipids (amino acids peptides and proteins) Apolipoprotein A1 Female Myelin-Oligodendrocyte Glycoprotein Neurology (clinical) Lipoprotein |
| Zdroj: | Journal of neuroimmunology. 277(1-2) |
| ISSN: | 1872-8421 |
| Popis: | Apolipoprotein A1 (Apo A-I), the most abundant component of high-density lipoprotein (HDL), is an anti-inflammatory molecule, yet its potential role in the pathogenesis of multiple sclerosis (MS) has not been fully investigated. In this study, Western blot analyses of human plasma showed differential Apo A-I expression in healthy controls compared to MS patients. Further, primary progressive MS patients had less plasma Apo A-I than other forms of MS. Using experimental allergic encephalomyelitis (EAE) as a model for MS, Apo A-I deficient mice exhibited worse clinical disease and more neurodegeneration concurrent with increased levels of pro-inflammatory cytokines compared to wild-type animals. These data suggest that Apo A-I plays a role in the pathogenesis of EAE, a model for MS, creating the possibility for agents that increase Apo A-I levels as potential therapies for MS. |
| Databáze: | OpenAIRE |
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