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  • 标题:Microparticles in multiple sclerosis and clinically isolated syndrome: effect on endothelial barrier function
  • 本地全文:下载
  • 作者:Beatriz Marcos-Ramiro ; Pedro Oliva Nacarino ; Esther Serrano-Pertierra
  • 期刊名称:BMC Neuroscience
  • 印刷版ISSN:1471-2202
  • 电子版ISSN:1471-2202
  • 出版年度:2014
  • 卷号:15
  • 期号:1
  • 页码:1
  • DOI:10.1186/1471-2202-15-110
  • 语种:English
  • 出版社:BioMed Central
  • 摘要: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.
  • 关键词:Multiple sclerosis ; Clinically isolated syndrome ; Microparticles ; Endothelial barrier function ; Thrombin
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