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ATP Release Guides Neutrophil Chemotaxis via P2Y2 and A3 Receptors
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 recep...
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Published in: | Science (American Association for the Advancement of Science) 2006-12, Vol.314 (5806), p.1792-1795 |
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creator | Chen, Yu Corriden, Ross Inoue, Yoshiaki Yip, Linda Hashiguchi, Naoyuki Zinkernagel, Annelies Nizet, Victor Insel, Paul A Junger, Wolfgang G |
description | 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. |
doi_str_mv | 10.1126/science.1132559 |
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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.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1132559</identifier><identifier>PMID: 17170310</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>Adenosine - metabolism ; Adenosine - pharmacology ; Adenosine A3 Receptor Agonists ; Adenosine A3 Receptor Antagonists ; Adenosine triphosphatase ; Adenosine Triphosphate - analogs & derivatives ; Adenosine Triphosphate - metabolism ; Adenosine Triphosphate - pharmacology ; Agonists ; Animal migration behavior ; Animals ; Autocrine Communication ; Bacteria ; Biological and medical sciences ; Cell adhesion & migration ; Cell Membrane - metabolism ; Cell membranes ; Cell physiology ; Cellular biology ; Chemotaxis ; Chemotaxis, Leukocyte - drug effects ; Cytoplasmic Granules - metabolism ; Fundamental and applied biological sciences. Psychology ; HL-60 Cells ; Humans ; Hydrolysis ; Leukocytes ; Mice ; Mice, Knockout ; Molecular and cellular biology ; Motility and taxis ; Neutrophils ; Neutrophils - drug effects ; Neutrophils - metabolism ; Neutrophils - physiology ; Phagocytes ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A3 - metabolism ; Receptors ; Receptors, Purinergic P2 - metabolism ; Receptors, Purinergic P2Y2 ; Signal amplification ; Signal Transduction ; Suramin - pharmacology</subject><ispartof>Science (American Association for the Advancement of Science), 2006-12, Vol.314 (5806), p.1792-1795</ispartof><rights>Copyright 2006 American Association for the Advancement of Science</rights><rights>2007 INIST-CNRS</rights><rights>Copyright American Association for the Advancement of Science Dec 15, 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-3b293782efb5ad027570a132a7f79b666f1c1e1ecb8f0e366690595a942ace203</citedby><cites>FETCH-LOGICAL-c588t-3b293782efb5ad027570a132a7f79b666f1c1e1ecb8f0e366690595a942ace203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/20035049$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/20035049$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,2870,2871,27903,27904,58217,58450</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18384786$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17170310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Yu</creatorcontrib><creatorcontrib>Corriden, Ross</creatorcontrib><creatorcontrib>Inoue, Yoshiaki</creatorcontrib><creatorcontrib>Yip, Linda</creatorcontrib><creatorcontrib>Hashiguchi, Naoyuki</creatorcontrib><creatorcontrib>Zinkernagel, Annelies</creatorcontrib><creatorcontrib>Nizet, Victor</creatorcontrib><creatorcontrib>Insel, Paul A</creatorcontrib><creatorcontrib>Junger, Wolfgang G</creatorcontrib><title>ATP Release Guides Neutrophil Chemotaxis via P2Y2 and A3 Receptors</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>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.</description><subject>Adenosine - metabolism</subject><subject>Adenosine - pharmacology</subject><subject>Adenosine A3 Receptor Agonists</subject><subject>Adenosine A3 Receptor Antagonists</subject><subject>Adenosine triphosphatase</subject><subject>Adenosine Triphosphate - analogs & derivatives</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Adenosine Triphosphate - pharmacology</subject><subject>Agonists</subject><subject>Animal migration behavior</subject><subject>Animals</subject><subject>Autocrine Communication</subject><subject>Bacteria</subject><subject>Biological and medical sciences</subject><subject>Cell adhesion & migration</subject><subject>Cell Membrane - metabolism</subject><subject>Cell membranes</subject><subject>Cell physiology</subject><subject>Cellular biology</subject><subject>Chemotaxis</subject><subject>Chemotaxis, Leukocyte - drug effects</subject><subject>Cytoplasmic Granules - metabolism</subject><subject>Fundamental and applied biological sciences. 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Psychology</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Hydrolysis</topic><topic>Leukocytes</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Molecular and cellular biology</topic><topic>Motility and taxis</topic><topic>Neutrophils</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - metabolism</topic><topic>Neutrophils - physiology</topic><topic>Phagocytes</topic><topic>Purinergic P2 Receptor Antagonists</topic><topic>Receptor, Adenosine A3 - metabolism</topic><topic>Receptors</topic><topic>Receptors, Purinergic P2 - metabolism</topic><topic>Receptors, Purinergic P2Y2</topic><topic>Signal amplification</topic><topic>Signal Transduction</topic><topic>Suramin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Yu</creatorcontrib><creatorcontrib>Corriden, Ross</creatorcontrib><creatorcontrib>Inoue, Yoshiaki</creatorcontrib><creatorcontrib>Yip, Linda</creatorcontrib><creatorcontrib>Hashiguchi, Naoyuki</creatorcontrib><creatorcontrib>Zinkernagel, Annelies</creatorcontrib><creatorcontrib>Nizet, Victor</creatorcontrib><creatorcontrib>Insel, Paul A</creatorcontrib><creatorcontrib>Junger, Wolfgang G</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aluminium Industry Abstracts</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Ceramic Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Computer and Information Systems Abstracts</collection><collection>Corrosion Abstracts</collection><collection>Ecology Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Materials Business File</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Engineering Research Database</collection><collection>Aerospace Database</collection><collection>Copper Technical Reference Library</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts – Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Immunology Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Yu</au><au>Corriden, Ross</au><au>Inoue, Yoshiaki</au><au>Yip, Linda</au><au>Hashiguchi, Naoyuki</au><au>Zinkernagel, Annelies</au><au>Nizet, Victor</au><au>Insel, Paul A</au><au>Junger, Wolfgang G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ATP Release Guides Neutrophil Chemotaxis via P2Y2 and A3 Receptors</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2006-12-15</date><risdate>2006</risdate><volume>314</volume><issue>5806</issue><spage>1792</spage><epage>1795</epage><pages>1792-1795</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><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.</abstract><cop>Washington, DC</cop><pub>American Association for the Advancement of Science</pub><pmid>17170310</pmid><doi>10.1126/science.1132559</doi><tpages>4</tpages></addata></record> |
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subjects | Adenosine - metabolism Adenosine - pharmacology Adenosine A3 Receptor Agonists Adenosine A3 Receptor Antagonists Adenosine triphosphatase Adenosine Triphosphate - analogs & derivatives Adenosine Triphosphate - metabolism Adenosine Triphosphate - pharmacology Agonists Animal migration behavior Animals Autocrine Communication Bacteria Biological and medical sciences Cell adhesion & migration Cell Membrane - metabolism Cell membranes Cell physiology Cellular biology Chemotaxis Chemotaxis, Leukocyte - drug effects Cytoplasmic Granules - metabolism Fundamental and applied biological sciences. Psychology HL-60 Cells Humans Hydrolysis Leukocytes Mice Mice, Knockout Molecular and cellular biology Motility and taxis Neutrophils Neutrophils - drug effects Neutrophils - metabolism Neutrophils - physiology Phagocytes Purinergic P2 Receptor Antagonists Receptor, Adenosine A3 - metabolism Receptors Receptors, Purinergic P2 - metabolism Receptors, Purinergic P2Y2 Signal amplification Signal Transduction Suramin - pharmacology |
title | ATP Release Guides Neutrophil Chemotaxis via P2Y2 and A3 Receptors |
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