IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms10363.html
   My bibliography  Save this article

Endomucin prevents leukocyte–endothelial cell adhesion and has a critical role under resting and inflammatory conditions

Author

Listed:
  • Alisar Zahr

    (Harvard Medical School)

  • Pilar Alcaide

    (Brigham and Women’s Hospital, Harvard Medical School
    Present address: Molecular Cardiology Research Institute, Tufts University School of Medicine, 800 Washington Street, Boston, Massachusetts 02111, USA.)

  • Jinling Yang

    (Harvard Medical School)

  • Alexander Jones

    (Harvard Medical School)

  • Meredith Gregory

    (Harvard Medical School)

  • Nathaniel G. dela Paz

    (Harvard Medical School)

  • Sunita Patel-Hett

    (Harvard Medical School)

  • Tania Nevers

    (Brigham and Women’s Hospital, Harvard Medical School
    Present address: Molecular Cardiology Research Institute, Tufts University School of Medicine, 800 Washington Street, Boston, Massachusetts 02111, USA.)

  • Adarsha Koirala

    (Harvard Medical School)

  • Francis W. Luscinskas

    (Brigham and Women’s Hospital, Harvard Medical School)

  • Magali Saint-Geniez

    (Harvard Medical School)

  • Bruce Ksander

    (Harvard Medical School)

  • Patricia A. D’Amore

    (Harvard Medical School
    Harvard Medical School)

  • Pablo Argüeso

    (Harvard Medical School)

Abstract

Endomucin is a membrane-bound glycoprotein expressed luminally by endothelial cells that line postcapillary venules, a primary site of leukocyte recruitment during inflammation. Here we show that endomucin abrogation on quiescent endothelial cells enables neutrophils to adhere firmly, via LFA-1-mediated binding to ICAM-1 constitutively expressed by endothelial cells. Moreover, TNF-α stimulation downregulates cell surface expression of endomucin concurrent with increased expression of adhesion molecules. Adenovirus-mediated expression of endomucin under inflammatory conditions prevents neutrophil adhesion in vitro and reduces the infiltration of CD45+ and NIMP-R14+ cells in vivo. These results indicate that endomucin prevents leukocyte contact with adhesion molecules in non-inflamed tissues and that downregulation of endomucin is critical to facilitate adhesion of leukocytes into inflamed tissues.

Suggested Citation

  • Alisar Zahr & Pilar Alcaide & Jinling Yang & Alexander Jones & Meredith Gregory & Nathaniel G. dela Paz & Sunita Patel-Hett & Tania Nevers & Adarsha Koirala & Francis W. Luscinskas & Magali Saint-Geni, 2016. "Endomucin prevents leukocyte–endothelial cell adhesion and has a critical role under resting and inflammatory conditions," Nature Communications, Nature, vol. 7(1), pages 1-10, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10363
    DOI: 10.1038/ncomms10363
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms10363
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms10363?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10363. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.