Microparticles in multiple sclerosis and clinically isolated syndrome: effect on endothelial barrier function
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- 作者：Beatriz Marcos-Ramiro (1)
Pedro Oliva Nacarino (2)
Esther Serrano-Pertierra (3)
Miguel 脕ngel Blanco-Gelaz (3)
Babette B Weksler (4)
Ignacio A Romero (5)
Pierre O Couraud (6)
Alberto Tu帽贸n (2)
Carlos L贸pez-Larrea (3)
Jaime Mill谩n (1)
Eva Cernuda-Moroll贸n (2)
1. Centro de Biolog铆a Molecular Severo Ochoa ; CSIC-UAM ; C/ Nicol谩s Cabrera 1 ; Cantoblanco ; 28049 ; Madrid ; Spain
2. Neurology Department ; Hospital Universitario Central de Asturias ; C/ Aldea Cerde帽o ; s/n ; 33011 ; Oviedo ; Spain
3. Immunology Department ; Hospital Universitario Central de Asturias ; Oviedo ; Spain
4. Weill Medical College of Cornell University ; New York ; NY ; USA
5. Department of Life Sciences ; The Open University ; Milton Keynes ; UK
6. Division of Hematology and Medical Oncology ; Institut Cochin ; Universit茅 Paris Descartes ; Paris ; France - 关键词：Multiple sclerosis ; Clinically isolated syndrome ; Microparticles ; Endothelial barrier function ; Thrombin
- 刊名：BMC Neuroscience
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：15
- 期：1
- 全文大小：2,913 KB
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- 出版者：BioMed Central
- ISSN：1471-2202
文摘
Background Cell-derived microparticles are secreted in response to cell damage or dysfunction. Endothelial and platelet dysfunction are thought to contribute to the development of multiple sclerosis (MS). Our aim here is, first, to compare the presence of microparticles of endothelial and platelet origin in plasma from patients with different clinical forms of MS and with clinically isolated syndrome. Second, to investigate the effect of microparticles on endothelial barrier function. Results Platelet-poor plasma from 95 patients (12 with clinically isolated syndrome, 51 relapsing-remitting, 23 secondary progressive, 9 primary progressive) and 49 healthy controls were analyzed for the presence of platelet-derived and endothelium-derived microparticles by flow cytometry. The plasma concentration of platelet-derived and endothelium-derived microparticles increased in all clinical forms of MS and in clinically isolated syndrome versus controls. The response of endothelial barriers to purified microparticles was measured by electric cell-substrate impedance sensing. Microparticles from relapsing-remitting MS patients induced, at equivalent concentrations, a stronger disruption of endothelial barriers than those from healthy donors or from patients with clinically isolated syndrome. MS microparticles acted synergistically with the inflammatory mediator thrombin to disrupt the endothelial barrier function. Conclusions Plasma microparticles should be considered not only as markers of early stages of MS, but also as pathological factors with the potential to increase endothelial permeability and leukocyte infiltration.