Blog
About

15
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      ATP release guides neutrophil chemotaxis via P2Y2 and A3 receptors.

      Science (New York, N.Y.)

      Adenosine, metabolism, pharmacology, Adenosine A3 Receptor Agonists, Adenosine A3 Receptor Antagonists, Adenosine Triphosphate, analogs & derivatives, Animals, Autocrine Communication, Cell Membrane, Chemotaxis, Leukocyte, drug effects, Cytoplasmic Granules, HL-60 Cells, Humans, Hydrolysis, Mice, Mice, Knockout, Neutrophils, physiology, Purinergic P2 Receptor Antagonists, Receptor, Adenosine A3, Receptors, Purinergic P2, Receptors, Purinergic P2Y2, Signal Transduction, Suramin

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Cells must amplify external signals to orient and migrate in chemotactic gradient fields. We find that human neutrophils release adenosine triphosphate (ATP) from the leading edge of the cell surface to amplify chemotactic signals and direct cell orientation by feedback through P2Y2 nucleotide receptors. Neutrophils rapidly hydrolyze released ATP to adenosine that then acts via A3-type adenosine receptors, which are recruited to the leading edge, to promote cell migration. Thus, ATP release and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling gradient sensing and migration of neutrophils.

          Related collections

          Author and article information

          Journal
          17170310
          10.1126/science.1132559

          Comments

          Comment on this article