Group IIA secretory phospholipase A₂ (GIIA) mediates apoptotic death during NMDA receptor activation in rat primary cortical neurons
J. Neurochem. (2010) 112, 1574-1583. Phospholipases A₂ (PLA₂) participate in neuronal death signalling pathways because of their ability to release lipid mediators, although the contribution of each isoform and mechanism of neurotoxicity are still elusive. Using a novel fluorogenic method to assess...
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| creator | Chiricozzi, Elena Fernandez-Fernandez, Seila Nardicchi, Vincenza Almeida, Angeles Bolaños, Juan Pedro Goracci, Gianfrancesco |
| description | J. Neurochem. (2010) 112, 1574-1583. Phospholipases A₂ (PLA₂) participate in neuronal death signalling pathways because of their ability to release lipid mediators, although the contribution of each isoform and mechanism of neurotoxicity are still elusive. Using a novel fluorogenic method to assess changes in a PLA₂ activity by flow cytometry, here we show that the group IIA secretory phospholipase A₂ isoform (GIIA) was specifically activated in cortical neurons following stimulation of N-methyl- d-aspartate glutamate receptor subtype (NMDAR). For activation, GIIA required Ca²⁺ and reactive oxygen/nitrogen species, and inhibition of its activity fully prevented NMDAR-mediated neuronal apoptotic death. Superoxide, nitric oxide or peroxynitrite donors stimulated GIIA activity, which mediated neuronal death. Intriguingly, we also found that GIIA activity induced mitochondrial superoxide production after NMDAR stimulation. These results reveal a novel role for GIIA in excitotoxicity both as target and producer of superoxide in a positive-loop of activation that may contribute to the propagation of neurodegeneration. |
| doi_str_mv | 10.1111/j.1471-4159.2010.06567.x |
| format | Article |
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Neurochem. (2010) 112, 1574-1583. Phospholipases A₂ (PLA₂) participate in neuronal death signalling pathways because of their ability to release lipid mediators, although the contribution of each isoform and mechanism of neurotoxicity are still elusive. Using a novel fluorogenic method to assess changes in a PLA₂ activity by flow cytometry, here we show that the group IIA secretory phospholipase A₂ isoform (GIIA) was specifically activated in cortical neurons following stimulation of N-methyl- d-aspartate glutamate receptor subtype (NMDAR). For activation, GIIA required Ca²⁺ and reactive oxygen/nitrogen species, and inhibition of its activity fully prevented NMDAR-mediated neuronal apoptotic death. Superoxide, nitric oxide or peroxynitrite donors stimulated GIIA activity, which mediated neuronal death. Intriguingly, we also found that GIIA activity induced mitochondrial superoxide production after NMDAR stimulation. These results reveal a novel role for GIIA in excitotoxicity both as target and producer of superoxide in a positive-loop of activation that may contribute to the propagation of neurodegeneration.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2010.06567.x</identifier><identifier>PMID: 20067579</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Ageing, cell death ; Animals ; Annexin A5 - metabolism ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Calcium - metabolism ; Cell physiology ; Cells, Cultured ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Cerebral Cortex - cytology ; Dose-Response Relationship, Drug ; Embryo, Mammalian ; Enzyme Inhibitors - pharmacology ; Excitatory Amino Acid Antagonists - pharmacology ; excitotoxicity ; Female ; Flow Cytometry - methods ; Fundamental and applied biological sciences. Psychology ; glutamate ; Glutamic Acid - pharmacology ; Group II Phospholipases A2 - metabolism ; Group II Phospholipases A2 - pharmacology ; Mitochondria - drug effects ; Mitochondria - metabolism ; Molecular and cellular biology ; Molsidomine - analogs & derivatives ; Molsidomine - pharmacology ; Neurodegeneration ; Neurology ; Neurons ; Neurons - drug effects ; Neurons - physiology ; Neurotoxicity ; Nitric Oxide Donors - pharmacology ; Nitroso Compounds - pharmacology ; Pregnancy ; primary cortical neurons ; Rats ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Receptors, N-Methyl-D-Aspartate - metabolism ; Rodents ; secretory phospholipase A ; secretory phospholipase A2 ; Vertebrates: nervous system and sense organs ; Xanthine - pharmacology ; Xanthine Oxidase - pharmacology</subject><ispartof>Journal of neurochemistry, 2010-03, Vol.112 (6), p.1574-1583</ispartof><rights>Journal Compilation © 2010 International Society for Neurochemistry. No claim to original US government works</rights><rights>2015 INIST-CNRS</rights><rights>Journal compilation © 2010 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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.1471-4159.2010.06567.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2010.06567.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22509600$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20067579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chiricozzi, Elena</creatorcontrib><creatorcontrib>Fernandez-Fernandez, Seila</creatorcontrib><creatorcontrib>Nardicchi, Vincenza</creatorcontrib><creatorcontrib>Almeida, Angeles</creatorcontrib><creatorcontrib>Bolaños, Juan Pedro</creatorcontrib><creatorcontrib>Goracci, Gianfrancesco</creatorcontrib><title>Group IIA secretory phospholipase A₂ (GIIA) mediates apoptotic death during NMDA receptor activation in rat primary cortical neurons</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>J. Neurochem. (2010) 112, 1574-1583. Phospholipases A₂ (PLA₂) participate in neuronal death signalling pathways because of their ability to release lipid mediators, although the contribution of each isoform and mechanism of neurotoxicity are still elusive. Using a novel fluorogenic method to assess changes in a PLA₂ activity by flow cytometry, here we show that the group IIA secretory phospholipase A₂ isoform (GIIA) was specifically activated in cortical neurons following stimulation of N-methyl- d-aspartate glutamate receptor subtype (NMDAR). For activation, GIIA required Ca²⁺ and reactive oxygen/nitrogen species, and inhibition of its activity fully prevented NMDAR-mediated neuronal apoptotic death. Superoxide, nitric oxide or peroxynitrite donors stimulated GIIA activity, which mediated neuronal death. Intriguingly, we also found that GIIA activity induced mitochondrial superoxide production after NMDAR stimulation. These results reveal a novel role for GIIA in excitotoxicity both as target and producer of superoxide in a positive-loop of activation that may contribute to the propagation of neurodegeneration.</description><subject>Ageing, cell death</subject><subject>Animals</subject><subject>Annexin A5 - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Calcium - metabolism</subject><subject>Cell physiology</subject><subject>Cells, Cultured</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Cerebral Cortex - cytology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Embryo, Mammalian</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>excitotoxicity</subject><subject>Female</subject><subject>Flow Cytometry - methods</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>glutamate</subject><subject>Glutamic Acid - pharmacology</subject><subject>Group II Phospholipases A2 - metabolism</subject><subject>Group II Phospholipases A2 - pharmacology</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Molecular and cellular biology</subject><subject>Molsidomine - analogs & derivatives</subject><subject>Molsidomine - pharmacology</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Neurotoxicity</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitroso Compounds - pharmacology</subject><subject>Pregnancy</subject><subject>primary cortical neurons</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Rodents</subject><subject>secretory phospholipase A</subject><subject>secretory phospholipase A2</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>Xanthine - pharmacology</subject><subject>Xanthine Oxidase - pharmacology</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkduO0zAQhi0EYsvCK4CFhICLlPE5ueCiKlCKlkXicG25jrPrKo2zdrKH273gQXkSHFoWCUuWLc_3z3jmRwgTmJO83mznhCtScCKqOYX8ClJINb--h2Z3gftoBkBpwYDTI_QopS0AkVySh-iIAkglVDVDP1cxjD1erxc4ORvdEOIN7s9Dyrv1vUkOL37d3uJXq4y8xjtXezO4hE0f-iEM3uLameEc12P03Rk-_fxugaOzLgcjNnbwl2bwocO-w9EMuI9-Z3IFG2LWmhZ3boyhS4_Rg8a0yT05nMfo64f335cfi5Mvq_VycVI0nDNVCFYLCYRUrhQApVFkI0tqQGwIB6cqxrhrGiotWCWYJZbzDbiacSp4w47Ry33SPoaL0aVB73yyrm1N58KYtOKSKgklZPL5f-Q2jLHLP9M0jxoEIzRDTw_QuMlz0Yfe9N_hZuDFATAp99pE01mf_nFUQCVhqvZ2z1351t3cxQnoyWy91ZOnevJUT2brP2bra_3pdDndsv7ZXt-YoM1ZzDV-fMskA1KCokKx3yxspYw</recordid><startdate>201003</startdate><enddate>201003</enddate><creator>Chiricozzi, Elena</creator><creator>Fernandez-Fernandez, Seila</creator><creator>Nardicchi, Vincenza</creator><creator>Almeida, Angeles</creator><creator>Bolaños, Juan Pedro</creator><creator>Goracci, Gianfrancesco</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</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>7QP</scope></search><sort><creationdate>201003</creationdate><title>Group IIA secretory phospholipase A₂ (GIIA) mediates apoptotic death during NMDA receptor activation in rat primary cortical neurons</title><author>Chiricozzi, Elena ; Fernandez-Fernandez, Seila ; Nardicchi, Vincenza ; Almeida, Angeles ; Bolaños, Juan Pedro ; Goracci, Gianfrancesco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-f4437-53d560119e85008a71b682a05b140e79334eff26c0c753c1c44b0ed34254f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Ageing, cell death</topic><topic>Animals</topic><topic>Annexin A5 - metabolism</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Calcium - metabolism</topic><topic>Cell physiology</topic><topic>Cells, Cultured</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Cerebral Cortex - cytology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Embryo, Mammalian</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>excitotoxicity</topic><topic>Female</topic><topic>Flow Cytometry - methods</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>glutamate</topic><topic>Glutamic Acid - pharmacology</topic><topic>Group II Phospholipases A2 - metabolism</topic><topic>Group II Phospholipases A2 - pharmacology</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Molecular and cellular biology</topic><topic>Molsidomine - analogs & derivatives</topic><topic>Molsidomine - pharmacology</topic><topic>Neurodegeneration</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Neurotoxicity</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitroso Compounds - pharmacology</topic><topic>Pregnancy</topic><topic>primary cortical neurons</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Rodents</topic><topic>secretory phospholipase A</topic><topic>secretory phospholipase A2</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>Xanthine - pharmacology</topic><topic>Xanthine Oxidase - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chiricozzi, Elena</creatorcontrib><creatorcontrib>Fernandez-Fernandez, Seila</creatorcontrib><creatorcontrib>Nardicchi, Vincenza</creatorcontrib><creatorcontrib>Almeida, Angeles</creatorcontrib><creatorcontrib>Bolaños, Juan Pedro</creatorcontrib><creatorcontrib>Goracci, Gianfrancesco</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>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>Calcium & Calcified Tissue Abstracts</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chiricozzi, Elena</au><au>Fernandez-Fernandez, Seila</au><au>Nardicchi, Vincenza</au><au>Almeida, Angeles</au><au>Bolaños, Juan Pedro</au><au>Goracci, Gianfrancesco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Group IIA secretory phospholipase A₂ (GIIA) mediates apoptotic death during NMDA receptor activation in rat primary cortical neurons</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2010-03</date><risdate>2010</risdate><volume>112</volume><issue>6</issue><spage>1574</spage><epage>1583</epage><pages>1574-1583</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>J. Neurochem. (2010) 112, 1574-1583. Phospholipases A₂ (PLA₂) participate in neuronal death signalling pathways because of their ability to release lipid mediators, although the contribution of each isoform and mechanism of neurotoxicity are still elusive. Using a novel fluorogenic method to assess changes in a PLA₂ activity by flow cytometry, here we show that the group IIA secretory phospholipase A₂ isoform (GIIA) was specifically activated in cortical neurons following stimulation of N-methyl- d-aspartate glutamate receptor subtype (NMDAR). For activation, GIIA required Ca²⁺ and reactive oxygen/nitrogen species, and inhibition of its activity fully prevented NMDAR-mediated neuronal apoptotic death. Superoxide, nitric oxide or peroxynitrite donors stimulated GIIA activity, which mediated neuronal death. Intriguingly, we also found that GIIA activity induced mitochondrial superoxide production after NMDAR stimulation. These results reveal a novel role for GIIA in excitotoxicity both as target and producer of superoxide in a positive-loop of activation that may contribute to the propagation of neurodegeneration.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>20067579</pmid><doi>10.1111/j.1471-4159.2010.06567.x</doi><tpages>10</tpages></addata></record> |
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| subjects | Ageing, cell death Animals Annexin A5 - metabolism Apoptosis Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Calcium - metabolism Cell physiology Cells, Cultured Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cerebral Cortex - cytology Dose-Response Relationship, Drug Embryo, Mammalian Enzyme Inhibitors - pharmacology Excitatory Amino Acid Antagonists - pharmacology excitotoxicity Female Flow Cytometry - methods Fundamental and applied biological sciences. Psychology glutamate Glutamic Acid - pharmacology Group II Phospholipases A2 - metabolism Group II Phospholipases A2 - pharmacology Mitochondria - drug effects Mitochondria - metabolism Molecular and cellular biology Molsidomine - analogs & derivatives Molsidomine - pharmacology Neurodegeneration Neurology Neurons Neurons - drug effects Neurons - physiology Neurotoxicity Nitric Oxide Donors - pharmacology Nitroso Compounds - pharmacology Pregnancy primary cortical neurons Rats Rats, Wistar Reactive Oxygen Species - metabolism Receptors, N-Methyl-D-Aspartate - metabolism Rodents secretory phospholipase A secretory phospholipase A2 Vertebrates: nervous system and sense organs Xanthine - pharmacology Xanthine Oxidase - pharmacology |
| title | Group IIA secretory phospholipase A₂ (GIIA) mediates apoptotic death during NMDA receptor activation in rat primary cortical neurons |
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