4.5 Article

Blood circulating microparticle species in relapsing-remitting and secondary progressive multiple sclerosis. A case-control, cross sectional study with conventional MRI and advanced iron content imaging outcomes

Journal

JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 355, Issue 1-2, Pages 84-89

Publisher

ELSEVIER
DOI: 10.1016/j.jns.2015.05.027

Keywords

Multiple sclerosis; Endothelial microparticles; MRI; Serum; Atrophy; Iron deposition

Funding

  1. Department of Defense [W81XWH-10-1-0717]
  2. National Institute of General Medical Sciences of the National Institutes of Health [P30GM110703]
  3. German Research Foundation (DFG) [BE 5619/1-1]

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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(+) (alpha V-3) 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 micropartide species in MS with conventional MRI (12- 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 micropartide 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. (C) 2015 Elsevier B.V. All rights reserved.

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