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Proteomic analysis of human cerebral endothelial cells activated by MS serum and IFN B‐1b
Author(s) -
Alexander J. Steven,
Jackson Sherry Robinson,
Jennings Merilyn H,
Minagar Alireza,
Wang Yuping
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a849-d
Subject(s) - angiogenin , multiple sclerosis , proteomics , endothelium , pathogenesis , endothelial stem cell , annexin a2 , interferon , blood–brain barrier , cell , medicine , immunology , biology , annexin , cancer research , angiogenesis , biochemistry , gene , central nervous system , in vitro
Several groups have recently described the endothelial cells (EC) as an important target of pathological mediators in multiple sclerosis (MS). Despite the recognition of the EC as a significant target in MS and a possible beneficiary of Beta‐interferon therapy, the structural changes which occur in the cerebrovascular endothelium and the effects of interferon‐â1b on these changes have not been closely evaluated. Disruption or dysregulation of the blood brain barrier (BBB) in MS represents a loss of endothelial integrity, which may facilitate the transendothelial migration of activated leukocytes responsible for the development of demyelinating lesions of MS. We used proteomics (2‐dimensional gel electrophoresis and MALDI‐MS) to characterize the effects of serum from MS patients with active disease (with and without interferon‐â1b therapy) on human cerebral endothelial cells. The results of this study revealed the up‐ and down‐regulation of expression of several proteins related to vascular development, cell structure, and cell cycle control. Using this approach we identified 14‐3‐3 ε, metavinculin, myosin‐9, plasminogen, reticulocalbin‐2 and‐3, ribonuclease/ angiogenin inhibitor 1, annexin A1, tropomyosin and Ras‐related protein Rap‐1A as potential new markers of active MS disease. A better understanding of the alterations within the cerebrovascular endothelium in MS pathogenesis of MS may lead to development of more potent therapies in MS. β