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MicroRNA-155 negatively affects blood-brain barrier function during neuroinflammation.

Author information

Affiliations

  • 1. Department of Life, Health, and Chemical Sciences, Biomedical Research Network, The Open University, Milton Keynes, UK;
      Authors
    • Lopez-Ramirez MA 1
    • Wu D 1
    • Hirst MC 1
    • Male DK 1
    • Romero IA 1
    (5 authors)
  • 2. Center for Neuroscience and Trauma, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK;
      Authors
    • Pryce G 2
    • King-Robson J 2
    • Kay O 2
    • Baker D 2
    • Michael GJ 2
    (5 authors)
  • 3. Sheffield Institute for Translational Neuroscience and.
      Authors
    • Simpson JE 3
    (1 author)
  • 4. Blood-Brain Barrier Research Group, Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
      Authors
    • Reijerkerk A 4
    • de Vries HE 4
    (2 authors)
  • 5. Department of Neurology, Sheffield Teaching Hospitals National Health Service (NHS) Trust, University of Sheffield, Sheffield, UK; and.
      Authors
    • Sharrack B 5
    (1 author)

ORCIDs linked to this article

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 06 Mar 2014, 28(6):2551-2565
https://doi.org/10.1096/fj.13-248880 PMID: 24604078 

Abstract 

Blood-brain barrier (BBB) dysfunction is a hallmark of neurological conditions such as multiple sclerosis (MS) and stroke. However, the molecular mechanisms underlying neurovascular dysfunction during BBB breakdown remain elusive. MicroRNAs (miRNAs) have recently emerged as key regulators of pathogenic responses, although their role in central nervous system (CNS) microvascular disorders is largely unknown. We have identified miR-155 as a critical miRNA in neuroinflammation at the BBB. miR-155 is expressed at the neurovascular unit of individuals with MS and of mice with experimental autoimmune encephalomyelitis (EAE). In mice, loss of miR-155 reduced CNS extravasation of systemic tracers, both in EAE and in an acute systemic inflammation model induced by lipopolysaccharide. In cultured human brain endothelium, miR-155 was strongly and rapidly upregulated by inflammatory cytokines. miR-155 up-regulation mimicked cytokine-induced alterations in junctional organization and permeability, whereas inhibition of endogenous miR-155 partially prevented a cytokine-induced increase in permeability. Furthermore, miR-155 modulated brain endothelial barrier function by targeting not only cell-cell complex molecules such as annexin-2 and claudin-1, but also focal adhesion components such as DOCK-1 and syntenin-1. We propose that brain endothelial miR-155 is a negative regulator of BBB function that may constitute a novel therapeutic target for CNS neuroinflammatory disorders.

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Read article at publisher's site: https://doi.org/10.1096/fj.13-248880

Read article for free, from open access legal sources, via Unpaywall: http://oro.open.ac.uk/42437/1/__science_Science-users_users_iar26_My%20Docs_Nacho_PAPERS_2013_FASEBJ-2013-248880v2-Romero.pdfUnpaywall

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Multiple Sclerosis Society of Canada