GABAergic striatal neurons exhibit caspase-independent, mitochondrially mediated programmed cell death
GABAergic striatal neurons are compromised in basal ganglia pathologies and we analysed how insult nature determined their patterns of injury and recruitment of the intrinsic mitochondrial pathway during programmed cell death (PCD). Stressors affecting targets implicated in striatal neurodegeneratio...
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| Veröffentlicht in: | Journal of neurochemistry 2009-05, Vol.109 (s1), p.198-206 |
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| creator | Diwakarla, Shanti Mercer, Linda D Kardashsyan, Liubov Chu, Percy W.Y Shin, Yea Seul Lau, Chew L Hughes, Maria L.R Nagley, Phillip Beart, Philip M |
| description | GABAergic striatal neurons are compromised in basal ganglia pathologies and we analysed how insult nature determined their patterns of injury and recruitment of the intrinsic mitochondrial pathway during programmed cell death (PCD). Stressors affecting targets implicated in striatal neurodegeneration [3-morpholinylsydnoneimine (SIN-1), 3-nitropropionic acid (3-NP), NMDA, 3,5-dihydroxyphenylglycine (DHPG), and staurosporine (STS)] were compared in cultured GABAergic neurons from murine striatum by analyzing the progression of injury and its correlation with mitochondrial involvement, the redistribution of intermembrane space (IMS) proteins, and patterns of protease activation. Stressors produced PCD exhibiting slow-onset kinetics with time-dependent annexin-V labeling and eventual DNA fragmentation. IMS proteins including cytochrome c were differentially distributed, although stressors except STS produced early redistribution of apoptosis-inducing factor and Omi, suggestive of early recruitment of both caspase-dependent and caspase-independent signaling. In general, Bax mobilization to mitochondria appeared to promote IMS protein redistribution. Caspase 3 activation was prominent after STS, whereas NMDA and SIN-1 produced mainly calpain activation, and 3-NP and DHPG elicited a mixed profile of protease activation. PCD and redistribution of IMS proteins in striatal GABAergic neurons were canonical and insult-dependent, reflecting differential interplay between the caspase cascade and alternate cell death pathways. |
| doi_str_mv | 10.1111/j.1471-4159.2009.05937.x |
| format | Article |
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Stressors affecting targets implicated in striatal neurodegeneration [3-morpholinylsydnoneimine (SIN-1), 3-nitropropionic acid (3-NP), NMDA, 3,5-dihydroxyphenylglycine (DHPG), and staurosporine (STS)] were compared in cultured GABAergic neurons from murine striatum by analyzing the progression of injury and its correlation with mitochondrial involvement, the redistribution of intermembrane space (IMS) proteins, and patterns of protease activation. Stressors produced PCD exhibiting slow-onset kinetics with time-dependent annexin-V labeling and eventual DNA fragmentation. IMS proteins including cytochrome c were differentially distributed, although stressors except STS produced early redistribution of apoptosis-inducing factor and Omi, suggestive of early recruitment of both caspase-dependent and caspase-independent signaling. In general, Bax mobilization to mitochondria appeared to promote IMS protein redistribution. Caspase 3 activation was prominent after STS, whereas NMDA and SIN-1 produced mainly calpain activation, and 3-NP and DHPG elicited a mixed profile of protease activation. PCD and redistribution of IMS proteins in striatal GABAergic neurons were canonical and insult-dependent, reflecting differential interplay between the caspase cascade and alternate cell death pathways.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2009.05937.x</identifier><identifier>PMID: 19393028</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Animals ; apoptogenic mitochondrial proteins ; apoptosis ; Apoptosis - physiology ; Bax ; Biochemistry ; calpain ; Calpain - metabolism ; caspase 3 ; Caspase 3 - metabolism ; Caspases - physiology ; Cell culture ; Cell Survival - drug effects ; Cell Survival - physiology ; Cells, Cultured ; death signaling ; DNA Fragmentation ; Enzyme Activation - physiology ; Female ; gamma-Aminobutyric Acid - physiology ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Mitochondria - drug effects ; Mitochondria - physiology ; Neostriatum - cytology ; Neostriatum - drug effects ; Neostriatum - physiology ; Neurology ; Neurons ; Neurons - drug effects ; Neurons - physiology ; Neurotransmitters ; Pregnancy ; programmed cell death</subject><ispartof>Journal of neurochemistry, 2009-05, Vol.109 (s1), p.198-206</ispartof><rights>2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry</rights><rights>Journal compilation © 2009 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5387-6e47dd771f9183786cda7cbde7c4e4d16c9fb7af1cae8c48ec46e5a02beedc593</citedby><cites>FETCH-LOGICAL-c5387-6e47dd771f9183786cda7cbde7c4e4d16c9fb7af1cae8c48ec46e5a02beedc593</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.1471-4159.2009.05937.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2009.05937.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,1434,27925,27926,45575,45576,46410,46834</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19393028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Diwakarla, Shanti</creatorcontrib><creatorcontrib>Mercer, Linda D</creatorcontrib><creatorcontrib>Kardashsyan, Liubov</creatorcontrib><creatorcontrib>Chu, Percy W.Y</creatorcontrib><creatorcontrib>Shin, Yea Seul</creatorcontrib><creatorcontrib>Lau, Chew L</creatorcontrib><creatorcontrib>Hughes, Maria L.R</creatorcontrib><creatorcontrib>Nagley, Phillip</creatorcontrib><creatorcontrib>Beart, Philip M</creatorcontrib><title>GABAergic striatal neurons exhibit caspase-independent, mitochondrially mediated programmed cell death</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>GABAergic striatal neurons are compromised in basal ganglia pathologies and we analysed how insult nature determined their patterns of injury and recruitment of the intrinsic mitochondrial pathway during programmed cell death (PCD). Stressors affecting targets implicated in striatal neurodegeneration [3-morpholinylsydnoneimine (SIN-1), 3-nitropropionic acid (3-NP), NMDA, 3,5-dihydroxyphenylglycine (DHPG), and staurosporine (STS)] were compared in cultured GABAergic neurons from murine striatum by analyzing the progression of injury and its correlation with mitochondrial involvement, the redistribution of intermembrane space (IMS) proteins, and patterns of protease activation. Stressors produced PCD exhibiting slow-onset kinetics with time-dependent annexin-V labeling and eventual DNA fragmentation. IMS proteins including cytochrome c were differentially distributed, although stressors except STS produced early redistribution of apoptosis-inducing factor and Omi, suggestive of early recruitment of both caspase-dependent and caspase-independent signaling. In general, Bax mobilization to mitochondria appeared to promote IMS protein redistribution. Caspase 3 activation was prominent after STS, whereas NMDA and SIN-1 produced mainly calpain activation, and 3-NP and DHPG elicited a mixed profile of protease activation. PCD and redistribution of IMS proteins in striatal GABAergic neurons were canonical and insult-dependent, reflecting differential interplay between the caspase cascade and alternate cell death pathways.</description><subject>Animals</subject><subject>apoptogenic mitochondrial proteins</subject><subject>apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Bax</subject><subject>Biochemistry</subject><subject>calpain</subject><subject>Calpain - metabolism</subject><subject>caspase 3</subject><subject>Caspase 3 - metabolism</subject><subject>Caspases - physiology</subject><subject>Cell culture</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cells, Cultured</subject><subject>death signaling</subject><subject>DNA Fragmentation</subject><subject>Enzyme Activation - physiology</subject><subject>Female</subject><subject>gamma-Aminobutyric Acid - physiology</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microscopy, Confocal</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - physiology</subject><subject>Neostriatum - cytology</subject><subject>Neostriatum - drug effects</subject><subject>Neostriatum - physiology</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Neurotransmitters</subject><subject>Pregnancy</subject><subject>programmed cell death</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkkuP0zAUhS0EYsrAXwCLBSsS_HayYNGpYACNYAGzthz7pnWVJsVORPvvcWgFEpupF37I3zm-uj4IYUpKmse7bUmFpoWgsi4ZIXVJZM11eXiEFn8vHqMFIYwVnAh2hZ6ltCWEKqHoU3RFa15zwqoFam-XN0uI6-BwGmOwo-1wD1Mc-oThsAlNGLGzaW8TFKH3sIc89eNbvAvj4DZD77Oo6454Bz6rweN9HNbR7vIZO-g67MGOm-foSWu7BC_O6zW6__jhx-pTcfft9vNqeVc4yStdKBDae61pW9OK60o5b7VrPGgnQHiqXN022rbUWaicqMAJBdIS1gB4l3twjd6cfHMVPydIo9mFNJdheximZJSmmkryMMiIUqwm-jJQ6-oCUApOqvnp1_-B22GKfW7LbCYlo5I_BFEm67m26gS5OKQUoTX7GHY2Hg0lZg6K2Zo5D2bOg5mDYv4ExRyy9OXZf2ryV_0TnpORgfcn4Ffo4HixsfnydTXvsv7VSd_awdh1DMncf2eE8hxCqjin_DeFitWl</recordid><startdate>200905</startdate><enddate>200905</enddate><creator>Diwakarla, Shanti</creator><creator>Mercer, Linda D</creator><creator>Kardashsyan, Liubov</creator><creator>Chu, Percy W.Y</creator><creator>Shin, Yea Seul</creator><creator>Lau, Chew L</creator><creator>Hughes, Maria L.R</creator><creator>Nagley, Phillip</creator><creator>Beart, Philip M</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><scope>FBQ</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>200905</creationdate><title>GABAergic striatal neurons exhibit caspase-independent, mitochondrially mediated programmed cell death</title><author>Diwakarla, Shanti ; 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Stressors affecting targets implicated in striatal neurodegeneration [3-morpholinylsydnoneimine (SIN-1), 3-nitropropionic acid (3-NP), NMDA, 3,5-dihydroxyphenylglycine (DHPG), and staurosporine (STS)] were compared in cultured GABAergic neurons from murine striatum by analyzing the progression of injury and its correlation with mitochondrial involvement, the redistribution of intermembrane space (IMS) proteins, and patterns of protease activation. Stressors produced PCD exhibiting slow-onset kinetics with time-dependent annexin-V labeling and eventual DNA fragmentation. IMS proteins including cytochrome c were differentially distributed, although stressors except STS produced early redistribution of apoptosis-inducing factor and Omi, suggestive of early recruitment of both caspase-dependent and caspase-independent signaling. In general, Bax mobilization to mitochondria appeared to promote IMS protein redistribution. Caspase 3 activation was prominent after STS, whereas NMDA and SIN-1 produced mainly calpain activation, and 3-NP and DHPG elicited a mixed profile of protease activation. PCD and redistribution of IMS proteins in striatal GABAergic neurons were canonical and insult-dependent, reflecting differential interplay between the caspase cascade and alternate cell death pathways.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>19393028</pmid><doi>10.1111/j.1471-4159.2009.05937.x</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals apoptogenic mitochondrial proteins apoptosis Apoptosis - physiology Bax Biochemistry calpain Calpain - metabolism caspase 3 Caspase 3 - metabolism Caspases - physiology Cell culture Cell Survival - drug effects Cell Survival - physiology Cells, Cultured death signaling DNA Fragmentation Enzyme Activation - physiology Female gamma-Aminobutyric Acid - physiology Membrane Proteins - metabolism Mice Mice, Inbred C57BL Microscopy, Confocal Mitochondria - drug effects Mitochondria - physiology Neostriatum - cytology Neostriatum - drug effects Neostriatum - physiology Neurology Neurons Neurons - drug effects Neurons - physiology Neurotransmitters Pregnancy programmed cell death |
| title | GABAergic striatal neurons exhibit caspase-independent, mitochondrially mediated programmed cell death |
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