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Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue

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  • معلومة اضافية
    • Publication Information:
      Hindawi Limited, 2013.
    • Publication Date:
      2013
    • Collection:
      Hindawi_Publishing_Corporation
      DOAJ-Articles_enriched
      European_Research_Council__ERC__enriched
      European_Research_Council__ERC
      DOAJ-Articles
      Crossref
      Hindawi_Publishing_Corporation_enriched
      Crossref_enriched
    • Abstract:
      Developmental endothelial locus-1 (Del-1) is an endothelial cell-secreted protein that limits the recruitment of neutrophils by antagonizing the interaction between the LFA-1 integrin on neutrophils and the intercellular adhesion molecule (ICAM)-1 on endothelial cells. Mice with genetic or age-associated Del-1 deficiency exhibit increased neutrophil infiltration in the periodontium resulting in inflammatory bone loss. Here we investigated additional novel mechanisms whereby Del-1 could interfere with neutrophil recruitment and inflammation. Treatment of human endothelial cells with Del-1 did not affect the expression of endothelial molecules involved in the leukocyte adhesion cascade (ICAM-1, VCAM-1, and E-selectin). Moreover, genetic or age-associated Del-1 deficiency did not significantly alter the expression of these adhesion molecules in the murine periodontium, further ruling out altered adhesion molecule expression as a mechanism whereby Del-1 regulates leukocyte recruitment. Strikingly, Del-1 inhibited ICAM-1-dependent chemokine release (CXCL2, CCL3) by neutrophils. Therefore, Del-1 could potentially suppress the amplification of inflammatory cell recruitment mediated through chemokine release by infiltrating neutrophils. Interestingly, Del-1 was itself regulated by inflammatory stimuli, which generally exerted opposite effects on adhesion molecule expression. The reciprocal regulation between Del-1 and inflammation may contribute to optimally balance the protective and the potentially harmful effects of inflammatory cell recruitment.
    • Accession Number:
      pmc: PMC3876683
      pmid: 24416060
    • File Description:
      text/xhtml
    • ISSN:
      1740-2530
      1740-2522
    • Accession Number:
      10.1155/2013/617809
    • Accession Number:
      edsair.dedup.wf.001..39c23b296bcf908d532fbf62c8b168e5