J S Alexander1, R Chervenak2, B Weinstock-Guttman3, I Tsunoda2, M Ramanathan4, N Martinez2, S Omura2, F Sato2, G V Chaitanya1, A Minagar5, J McGee6, M H Jennings1, C Monceaux1, F Becker7, U Cvek8, M Trutschl8, R Zivadinov9. 1. Department of Molecular and Cellular Physiology, Louisiana State University Health-Shreveport, LA, USA. 2. Department Microbiology & Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health-Shreveport, LA, USA. 3. The Jacobs Neurological Institute, Department of Neurology, University of Buffalo, Buffalo, NY, USA. 4. Department of Pharmaceutical Sciences, State University of New York, Buffalo, NY, USA. 5. Department of Neurology, Louisiana State University Health-Shreveport, LA, USA. Electronic address: aminag@lsuhsc.edu. 6. Department of Neurology, Louisiana State University Health-Shreveport, LA, USA. 7. Department of Molecular and Cellular Physiology, Louisiana State University Health-Shreveport, LA, USA; Department for General and Visceral Surgery, Muenster, Germany. 8. Computer Sciences Department, Louisiana State University-Shreveport, LA, USA. 9. The Jacobs Neurological Institute, Department of Neurology, University of Buffalo, Buffalo, NY, USA; Buffalo Neuroimaging Analysis Center, Department of Neurology, University of Buffalo, Buffalo, NY, USA.
Abstract
BACKGROUND: Although multiple sclerosis (MS) is thought to represent an excessive and inappropriate immune response to several central nervous system (CNS) autoantigens, increasing evidence also suggests that MS may also be a neurovascular inflammatory disease, characterized by endothelial activation and shedding of cell membrane microdomains known as 'microparticles' into the circulation. OBJECTIVE: To investigate the relationships between these endothelial biomarkers and MS. METHODS: We examined the relative abundance of CD31(+)/PECAM-1, CD51(+)CD61(+) (αV-β3) and CD54(+) (ICAM-1) bearing microparticles in sera of healthy individuals, patients with relapsing-remitting MS, and secondary-progressive MS. We also investigated the correlation among circulating levels of different microparticle species in MS with conventional MRI (T2- and T1-lesion volumes and brain atrophy), as well as novel MR modalities [assessment of iron content on susceptibility-weighted imaging (SWI)-filtered phase]. RESULTS: Differences in circulating microparticle levels were found among MS groups, and several microparticle species (CD31(+)/CD51(+)/CD61(+)/CD54(+)) were found to correlate with conventional MRI and SWI features of MS. CONCLUSION: These results indicate that circulating microparticles' profiles in MS may support mechanistic roles for microvascular stress and injury which is an underlying contributor not only to MS initiation and progression, but also to pro-inflammatory responses.
BACKGROUND: Although multiple sclerosis (MS) is thought to represent an excessive and inappropriate immune response to several central nervous system (CNS) autoantigens, increasing evidence also suggests that MS may also be a neurovascular inflammatory disease, characterized by endothelial activation and shedding of cell membrane microdomains known as 'microparticles' into the circulation. OBJECTIVE: To investigate the relationships between these endothelial biomarkers and MS. METHODS: We examined the relative abundance of CD31(+)/PECAM-1, CD51(+)CD61(+) (αV-β3) and CD54(+) (ICAM-1) bearing microparticles in sera of healthy individuals, patients with relapsing-remitting MS, and secondary-progressive MS. We also investigated the correlation among circulating levels of different microparticle species in MS with conventional MRI (T2- and T1-lesion volumes and brain atrophy), as well as novel MR modalities [assessment of iron content on susceptibility-weighted imaging (SWI)-filtered phase]. RESULTS: Differences in circulating microparticle levels were found among MS groups, and several microparticle species (CD31(+)/CD51(+)/CD61(+)/CD54(+)) were found to correlate with conventional MRI and SWI features of MS. CONCLUSION: These results indicate that circulating microparticles' profiles in MS may support mechanistic roles for microvascular stress and injury which is an underlying contributor not only to MS initiation and progression, but also to pro-inflammatory responses.
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