Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration
J. Neurochem. (2012) 121, 217–227. The extension of microglial processes toward injured sites in the brain is triggered by the stimulation of the purinergic receptor P2Y12 by extracellular ATP. We recently showed that P2Y12 stimulation by ATP induces microglial process extension in collagen gels. In...
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| description | J. Neurochem. (2012) 121, 217–227.
The extension of microglial processes toward injured sites in the brain is triggered by the stimulation of the purinergic receptor P2Y12 by extracellular ATP. We recently showed that P2Y12 stimulation by ATP induces microglial process extension in collagen gels. In the present study, we found that a P2Y12 agonist, 2‐methylthio‐ADP (2MeSADP), failed to induce the process extension of microglia in collagen gels and that co‐stimulation with adenosine, a phosphohydrolytic derivative of ATP, and 2MeSADP restored the chemotactic process extension. An adenosine A3 receptor (A3R)‐selective agonist restored the chemotactic process extension, but other receptor subtype agonists did not. The removal of adenosine by adenosine deaminase and the blocking of A3R by an A3R‐selective antagonist inhibited ADP‐induced process extension. The A3R antagonist inhibited ADP‐induced microglial migration, and an A3R agonist promoted 2MeSADP‐stimulated migration. ADP and the A3R agonist activated Jun N‐terminal kinase in microglia, and a Jun N‐terminal kinase inhibitor inhibited the ADP‐induced process extension. An RT‐PCR analysis showed that A1R and A3R were expressed by microglia sorted from adult rat brains and that the A2AR expression level was very low. These results suggested that A3R signaling may be involved in the ADP‐induced process extension and migration of microglia.
Process extension and migration of microglia towards injured sites in the brain are triggered by the stimulation of the purinergic receptor P2Y12 with extracellular ATP. Our results indicate that adenosine, a phosphohydrolytic derivative of ATP, promoted P2Y12‐mediated process extension and migration through the adenosine A3 receptor. These findings suggest that A3 signaling cooperates with P2Y12 to regulate the chemotactic motion of microglia in response to neuronal damage. |
| doi_str_mv | 10.1111/j.1471-4159.2012.07693.x |
| format | Article |
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The extension of microglial processes toward injured sites in the brain is triggered by the stimulation of the purinergic receptor P2Y12 by extracellular ATP. We recently showed that P2Y12 stimulation by ATP induces microglial process extension in collagen gels. In the present study, we found that a P2Y12 agonist, 2‐methylthio‐ADP (2MeSADP), failed to induce the process extension of microglia in collagen gels and that co‐stimulation with adenosine, a phosphohydrolytic derivative of ATP, and 2MeSADP restored the chemotactic process extension. An adenosine A3 receptor (A3R)‐selective agonist restored the chemotactic process extension, but other receptor subtype agonists did not. The removal of adenosine by adenosine deaminase and the blocking of A3R by an A3R‐selective antagonist inhibited ADP‐induced process extension. The A3R antagonist inhibited ADP‐induced microglial migration, and an A3R agonist promoted 2MeSADP‐stimulated migration. ADP and the A3R agonist activated Jun N‐terminal kinase in microglia, and a Jun N‐terminal kinase inhibitor inhibited the ADP‐induced process extension. An RT‐PCR analysis showed that A1R and A3R were expressed by microglia sorted from adult rat brains and that the A2AR expression level was very low. These results suggested that A3R signaling may be involved in the ADP‐induced process extension and migration of microglia.
Process extension and migration of microglia towards injured sites in the brain are triggered by the stimulation of the purinergic receptor P2Y12 with extracellular ATP. Our results indicate that adenosine, a phosphohydrolytic derivative of ATP, promoted P2Y12‐mediated process extension and migration through the adenosine A3 receptor. These findings suggest that A3 signaling cooperates with P2Y12 to regulate the chemotactic motion of microglia in response to neuronal damage.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2012.07693.x</identifier><identifier>PMID: 22335470</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adenosine ; Adenosine - pharmacology ; Adenosine A3 Receptor Agonists - pharmacology ; Adenosine A3 receptors ; Adenosine deaminase ; Adenosine Deaminase Inhibitors - pharmacology ; Adenosine Diphosphate - analogs & derivatives ; Adenosine Diphosphate - pharmacology ; Adult and adolescent clinical studies ; Animals ; Animals, Newborn ; ATP ; Biological and medical sciences ; Brain ; Cell adhesion & migration ; Cell migration ; Cell Movement - drug effects ; Cells, Cultured ; Cerebral Cortex - cytology ; Cerebral Cortex - drug effects ; chemotaxis ; Chemotaxis - drug effects ; Collagen ; Enzymes ; Flow Cytometry ; Gels ; Indicators and Reagents ; Injuries of the nervous system and the skull. Diseases due to physical agents ; JNK Mitogen-Activated Protein Kinases - physiology ; Medical sciences ; Microglia ; Microglia - drug effects ; motility ; Neurochemistry ; Neurons ; Organic mental disorders. Neuropsychology ; P2Y12 ; Polymerase chain reaction ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Purine receptors ; purinergic ; Purinergic P2Y Receptor Agonists - pharmacology ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Receptor, Adenosine A1 - biosynthesis ; Receptor, Adenosine A3 - drug effects ; Receptor, Adenosine A3 - physiology ; Receptors, Purinergic P2Y12 - drug effects ; Thionucleotides - pharmacology ; Traumas. Diseases due to physical agents</subject><ispartof>Journal of neurochemistry, 2012-04, Vol.121 (2), p.217-227</ispartof><rights>2012 The Authors. Journal of Neurochemistry © 2012 International Society for Neurochemistry</rights><rights>2015 INIST-CNRS</rights><rights>2012 The Authors. Journal of Neurochemistry © 2012 International Society for Neurochemistry.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6123-9ed6e7b66e71898b25ba4cfbaac69a048908ddc796a245c99645d68ff37028843</citedby><cites>FETCH-LOGICAL-c6123-9ed6e7b66e71898b25ba4cfbaac69a048908ddc796a245c99645d68ff37028843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2012.07693.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2012.07693.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25811377$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22335470$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ohsawa, Keiko</creatorcontrib><creatorcontrib>Sanagi, Tomomi</creatorcontrib><creatorcontrib>Nakamura, Yasuko</creatorcontrib><creatorcontrib>Suzuki, Eri</creatorcontrib><creatorcontrib>Inoue, Kazuhide</creatorcontrib><creatorcontrib>Kohsaka, Shinichi</creatorcontrib><title>Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>J. Neurochem. (2012) 121, 217–227.
The extension of microglial processes toward injured sites in the brain is triggered by the stimulation of the purinergic receptor P2Y12 by extracellular ATP. We recently showed that P2Y12 stimulation by ATP induces microglial process extension in collagen gels. In the present study, we found that a P2Y12 agonist, 2‐methylthio‐ADP (2MeSADP), failed to induce the process extension of microglia in collagen gels and that co‐stimulation with adenosine, a phosphohydrolytic derivative of ATP, and 2MeSADP restored the chemotactic process extension. An adenosine A3 receptor (A3R)‐selective agonist restored the chemotactic process extension, but other receptor subtype agonists did not. The removal of adenosine by adenosine deaminase and the blocking of A3R by an A3R‐selective antagonist inhibited ADP‐induced process extension. The A3R antagonist inhibited ADP‐induced microglial migration, and an A3R agonist promoted 2MeSADP‐stimulated migration. ADP and the A3R agonist activated Jun N‐terminal kinase in microglia, and a Jun N‐terminal kinase inhibitor inhibited the ADP‐induced process extension. An RT‐PCR analysis showed that A1R and A3R were expressed by microglia sorted from adult rat brains and that the A2AR expression level was very low. These results suggested that A3R signaling may be involved in the ADP‐induced process extension and migration of microglia.
Process extension and migration of microglia towards injured sites in the brain are triggered by the stimulation of the purinergic receptor P2Y12 with extracellular ATP. Our results indicate that adenosine, a phosphohydrolytic derivative of ATP, promoted P2Y12‐mediated process extension and migration through the adenosine A3 receptor. These findings suggest that A3 signaling cooperates with P2Y12 to regulate the chemotactic motion of microglia in response to neuronal damage.</description><subject>Adenosine</subject><subject>Adenosine - pharmacology</subject><subject>Adenosine A3 Receptor Agonists - pharmacology</subject><subject>Adenosine A3 receptors</subject><subject>Adenosine deaminase</subject><subject>Adenosine Deaminase Inhibitors - pharmacology</subject><subject>Adenosine Diphosphate - analogs & derivatives</subject><subject>Adenosine Diphosphate - pharmacology</subject><subject>Adult and adolescent clinical studies</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>ATP</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - drug effects</subject><subject>chemotaxis</subject><subject>Chemotaxis - drug effects</subject><subject>Collagen</subject><subject>Enzymes</subject><subject>Flow Cytometry</subject><subject>Gels</subject><subject>Indicators and Reagents</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>JNK Mitogen-Activated Protein Kinases - physiology</subject><subject>Medical sciences</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>motility</subject><subject>Neurochemistry</subject><subject>Neurons</subject><subject>Organic mental disorders. Neuropsychology</subject><subject>P2Y12</subject><subject>Polymerase chain reaction</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Purine receptors</subject><subject>purinergic</subject><subject>Purinergic P2Y Receptor Agonists - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptor, Adenosine A1 - biosynthesis</subject><subject>Receptor, Adenosine A3 - drug effects</subject><subject>Receptor, Adenosine A3 - physiology</subject><subject>Receptors, Purinergic P2Y12 - drug effects</subject><subject>Thionucleotides - pharmacology</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUuP0zAUhS0EYkrhLyALCcEmwa_4sWBROjDMMCoIgUBiYTmOM3JJnY6dDJ1_j0NLkVggvLDvlb9zdO0DAMSoxHm9WJeYCVwwXKmSIExKJLii5e4OmB0v7oIZQoQUFDFyAh6ktEYIc8bxfXBCCKUVE2gGvi0aF_rkg4MLCqOzbjv0EfoEfbjpuxvX5AIuTj8UPjSjze3G29hfdd50cBt761KCbje4kHwfoAkTcBXNkLuH4F5ruuQeHc45-Pzm9afl2-Ly_dn5cnFZWI4JLZRruBM1zxuWStakqg2zbW2M5cogJhWSTWOF4oawyirFWdVw2bZUICIlo3PwbO-b57keXRr0xifrus4E149JK0UpllyRTD7_J4kRyoZcCJrRJ3-h636MIb9D5wEQFpWY_OQeyl-SUnSt3ka_MfE2O-kpKb3WUyB6CkRPSelfSeldlj4--I_1xjVH4e9oMvD0AJhkTddGE6xPf7hKYkzzpHPwcs_98J27_e8B9MVqOVVZX-z1Pg1ud9Sb-F1zQUWlv6zO9Luvy1fkIyN6RX8CHuS8Lw</recordid><startdate>201204</startdate><enddate>201204</enddate><creator>Ohsawa, Keiko</creator><creator>Sanagi, Tomomi</creator><creator>Nakamura, Yasuko</creator><creator>Suzuki, Eri</creator><creator>Inoue, Kazuhide</creator><creator>Kohsaka, Shinichi</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201204</creationdate><title>Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration</title><author>Ohsawa, Keiko ; Sanagi, Tomomi ; Nakamura, Yasuko ; Suzuki, Eri ; Inoue, Kazuhide ; Kohsaka, Shinichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6123-9ed6e7b66e71898b25ba4cfbaac69a048908ddc796a245c99645d68ff37028843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenosine</topic><topic>Adenosine - pharmacology</topic><topic>Adenosine A3 Receptor Agonists - pharmacology</topic><topic>Adenosine A3 receptors</topic><topic>Adenosine deaminase</topic><topic>Adenosine Deaminase Inhibitors - pharmacology</topic><topic>Adenosine Diphosphate - analogs & derivatives</topic><topic>Adenosine Diphosphate - pharmacology</topic><topic>Adult and adolescent clinical studies</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>ATP</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Cell adhesion & migration</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - drug effects</topic><topic>chemotaxis</topic><topic>Chemotaxis - drug effects</topic><topic>Collagen</topic><topic>Enzymes</topic><topic>Flow Cytometry</topic><topic>Gels</topic><topic>Indicators and Reagents</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>JNK Mitogen-Activated Protein Kinases - physiology</topic><topic>Medical sciences</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>motility</topic><topic>Neurochemistry</topic><topic>Neurons</topic><topic>Organic mental disorders. Neuropsychology</topic><topic>P2Y12</topic><topic>Polymerase chain reaction</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Purine receptors</topic><topic>purinergic</topic><topic>Purinergic P2Y Receptor Agonists - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptor, Adenosine A1 - biosynthesis</topic><topic>Receptor, Adenosine A3 - drug effects</topic><topic>Receptor, Adenosine A3 - physiology</topic><topic>Receptors, Purinergic P2Y12 - drug effects</topic><topic>Thionucleotides - pharmacology</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ohsawa, Keiko</creatorcontrib><creatorcontrib>Sanagi, Tomomi</creatorcontrib><creatorcontrib>Nakamura, Yasuko</creatorcontrib><creatorcontrib>Suzuki, Eri</creatorcontrib><creatorcontrib>Inoue, Kazuhide</creatorcontrib><creatorcontrib>Kohsaka, Shinichi</creatorcontrib><collection>Istex</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ohsawa, Keiko</au><au>Sanagi, Tomomi</au><au>Nakamura, Yasuko</au><au>Suzuki, Eri</au><au>Inoue, Kazuhide</au><au>Kohsaka, Shinichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2012-04</date><risdate>2012</risdate><volume>121</volume><issue>2</issue><spage>217</spage><epage>227</epage><pages>217-227</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>J. Neurochem. (2012) 121, 217–227.
The extension of microglial processes toward injured sites in the brain is triggered by the stimulation of the purinergic receptor P2Y12 by extracellular ATP. We recently showed that P2Y12 stimulation by ATP induces microglial process extension in collagen gels. In the present study, we found that a P2Y12 agonist, 2‐methylthio‐ADP (2MeSADP), failed to induce the process extension of microglia in collagen gels and that co‐stimulation with adenosine, a phosphohydrolytic derivative of ATP, and 2MeSADP restored the chemotactic process extension. An adenosine A3 receptor (A3R)‐selective agonist restored the chemotactic process extension, but other receptor subtype agonists did not. The removal of adenosine by adenosine deaminase and the blocking of A3R by an A3R‐selective antagonist inhibited ADP‐induced process extension. The A3R antagonist inhibited ADP‐induced microglial migration, and an A3R agonist promoted 2MeSADP‐stimulated migration. ADP and the A3R agonist activated Jun N‐terminal kinase in microglia, and a Jun N‐terminal kinase inhibitor inhibited the ADP‐induced process extension. An RT‐PCR analysis showed that A1R and A3R were expressed by microglia sorted from adult rat brains and that the A2AR expression level was very low. These results suggested that A3R signaling may be involved in the ADP‐induced process extension and migration of microglia.
Process extension and migration of microglia towards injured sites in the brain are triggered by the stimulation of the purinergic receptor P2Y12 with extracellular ATP. Our results indicate that adenosine, a phosphohydrolytic derivative of ATP, promoted P2Y12‐mediated process extension and migration through the adenosine A3 receptor. These findings suggest that A3 signaling cooperates with P2Y12 to regulate the chemotactic motion of microglia in response to neuronal damage.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22335470</pmid><doi>10.1111/j.1471-4159.2012.07693.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Adenosine - pharmacology Adenosine A3 Receptor Agonists - pharmacology Adenosine A3 receptors Adenosine deaminase Adenosine Deaminase Inhibitors - pharmacology Adenosine Diphosphate - analogs & derivatives Adenosine Diphosphate - pharmacology Adult and adolescent clinical studies Animals Animals, Newborn ATP Biological and medical sciences Brain Cell adhesion & migration Cell migration Cell Movement - drug effects Cells, Cultured Cerebral Cortex - cytology Cerebral Cortex - drug effects chemotaxis Chemotaxis - drug effects Collagen Enzymes Flow Cytometry Gels Indicators and Reagents Injuries of the nervous system and the skull. Diseases due to physical agents JNK Mitogen-Activated Protein Kinases - physiology Medical sciences Microglia Microglia - drug effects motility Neurochemistry Neurons Organic mental disorders. Neuropsychology P2Y12 Polymerase chain reaction Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Purine receptors purinergic Purinergic P2Y Receptor Agonists - pharmacology Rats Rats, Wistar Real-Time Polymerase Chain Reaction Receptor, Adenosine A1 - biosynthesis Receptor, Adenosine A3 - drug effects Receptor, Adenosine A3 - physiology Receptors, Purinergic P2Y12 - drug effects Thionucleotides - pharmacology Traumas. Diseases due to physical agents |
| title | Adenosine A3 receptor is involved in ADP-induced microglial process extension and migration |
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