VAMP-8 segregates mast cell–preformed mediator exocytosis from cytokine trafficking pathways

  • Neeraj Tiwari
    Inserm U699, Paris, France;
  • Cheng-Chun Wang
    Membrane Biology Laboratory, Institute of Molecular and Cellular Biology, Proteos, Singapore;
  • Cristiana Brochetta
    Inserm U699, Paris, France;
  • Gou Ke
    Membrane Biology Laboratory, Institute of Molecular and Cellular Biology, Proteos, Singapore;
  • Francesca Vita
    Department of Physiology and Pathology, University of Trieste, Trieste, Italy; and
  • Zeng Qi
    Membrane Biology Laboratory, Institute of Molecular and Cellular Biology, Proteos, Singapore;
  • Juan Rivera
    Laboratory of Immune Cell Signaling, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD
  • Maria Rosa Soranzo
    Department of Physiology and Pathology, University of Trieste, Trieste, Italy; and
  • Giuliano Zabucchi
    Department of Physiology and Pathology, University of Trieste, Trieste, Italy; and
  • Wanjin Hong
    Membrane Biology Laboratory, Institute of Molecular and Cellular Biology, Proteos, Singapore;
  • Ulrich Blank
    Inserm U699, Paris, France;

書誌事項

公開日
2008-04-01
DOI
  • 10.1182/blood-2007-07-103309
公開者
American Society of Hematology

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説明

<jats:title>Abstract</jats:title><jats:p>Inflammatory responses by mast cells are characterized by massive exocytosis of prestored granular mediators followed by cytokine/chemokine release. The vesicular trafficking mechanisms involved remain poorly understood. Vesicular-associated membrane protein-8 (VAMP-8), a member of the soluble N-ethylmaleimide–sensitive factor (NSF) attachment protein receptor (SNARE) family of fusion proteins initially characterized in endosomal and endosomal-lysosomal fusion, may also function in regulated exocytosis. Here we show that in bone marrow–derived mast cells (BMMCs) VAMP-8 partially colocalized with secretory granules and redistributed upon stimulation. This was associated with increased SNARE complex formation with the target t-SNAREs, SNAP-23 and syntaxin-4. VAMP-8–deficient BMMCs exhibited a markedly reduced degranulation response after IgE+ antigen-, thapsigargin-, or ionomycin-induced stimulation. VAMP-8–deficient mice also showed reduced plasma histamine levels in passive systemic anaphylaxis experiments, while cytokine/chemokine release was not affected. Unprocessed TNF accumulated at the plasma membrane where it colocalized with a VAMP-3–positive vesicular compartment but not with VAMP-8. The findings demonstrate that VAMP-8 segregates secretory lysosomal granule exocytosis in mast cells from cytokine/chemokine molecular trafficking pathways.</jats:p>

収録刊行物

  • Blood

    Blood 111 (7), 3665-3674, 2008-04-01

    American Society of Hematology

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