p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca2+ homeostasis
p66Shc, a redox enzyme that enhances reactive oxygen species (ROS) production by mitochondria, promotes T cell apoptosis. We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca2+]c. p66Shc expression resulted in profound mitoc...
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| Veröffentlicht in: | Cell death and differentiation 2007-02, Vol.14 (2), p.338-347 |
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| container_title | Cell death and differentiation |
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| creator | Pellegrini, M Finetti, F Petronilli, V Ulivieri, C Giusti, F Lupetti, P Giorgio, M Pelicci, P G Bernardi, P Baldari, C T |
| description | p66Shc, a redox enzyme that enhances reactive oxygen species (ROS) production by mitochondria, promotes T cell apoptosis. We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca2+]c. p66Shc expression resulted in profound mitochondrial dysfunction in response to the Ca2+ ionophore A23187, as revealed by dissipation of mitochondrial transmembrane potential, cytochrome c release and decreased ATP levels. p66Shc expression also caused a dramatic alteration in the cells' Ca2+-handling ability, which resulted in Ca2+ overload after A23187 treatment. The impairment in Ca2+ homeostasis was ROS dependent and caused by defective Ca2+ extrusion due at least in part to decreased plasma membrane ATPase (PMCA) expression. Both effects of p66Shc required Ca2+-dependent serine-36 phosphorylation. The mitochondrial effects of p66Shc were potentiated by but not strictly dependent on the rise in [Ca2+]c. Thus, Ca2+-dependent p66Shc phosphorylation causes both mitochondrial dysfunction and impaired Ca2+ homeostasis, which synergize in promoting T cell apoptosis. |
| doi_str_mv | 10.1038/sj.cdd.4401997 |
| format | Article |
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We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca2+]c. p66Shc expression resulted in profound mitochondrial dysfunction in response to the Ca2+ ionophore A23187, as revealed by dissipation of mitochondrial transmembrane potential, cytochrome c release and decreased ATP levels. p66Shc expression also caused a dramatic alteration in the cells' Ca2+-handling ability, which resulted in Ca2+ overload after A23187 treatment. The impairment in Ca2+ homeostasis was ROS dependent and caused by defective Ca2+ extrusion due at least in part to decreased plasma membrane ATPase (PMCA) expression. Both effects of p66Shc required Ca2+-dependent serine-36 phosphorylation. The mitochondrial effects of p66Shc were potentiated by but not strictly dependent on the rise in [Ca2+]c. Thus, Ca2+-dependent p66Shc phosphorylation causes both mitochondrial dysfunction and impaired Ca2+ homeostasis, which synergize in promoting T cell apoptosis.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/sj.cdd.4401997</identifier><identifier>PMID: 16794602</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Adaptor Proteins, Signal Transducing - metabolism ; Apoptosis ; Apoptosis - drug effects ; Calcimycin - pharmacology ; Calcium - metabolism ; Cell death ; Cytochrome ; Down-Regulation - drug effects ; Enzymes ; Evolutionary biology ; Flow Cytometry ; Gene Expression Regulation, Enzymologic - drug effects ; Homeostasis ; Homeostasis - drug effects ; Humans ; Jurkat Cells ; Kinases ; Lymphocytes ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - enzymology ; Mitochondria - metabolism ; Oncology ; Oxidative stress ; Permeability ; Phosphorylation ; Phosphoserine - metabolism ; Plasma ; Plasma Membrane Calcium-Transporting ATPases - genetics ; Reactive Oxygen Species - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Shc Signaling Adaptor Proteins ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; T-Lymphocytes - cytology ; T-Lymphocytes - drug effects ; T-Lymphocytes - immunology ; T-Lymphocytes - ultrastructure</subject><ispartof>Cell death and differentiation, 2007-02, Vol.14 (2), p.338-347</ispartof><rights>Copyright Nature Publishing Group Feb 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c290t-232ad64f16ce441676f4d3792545046905aa1326880fde104711a733c26a4c793</citedby><cites>FETCH-LOGICAL-c290t-232ad64f16ce441676f4d3792545046905aa1326880fde104711a733c26a4c793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16794602$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pellegrini, M</creatorcontrib><creatorcontrib>Finetti, F</creatorcontrib><creatorcontrib>Petronilli, V</creatorcontrib><creatorcontrib>Ulivieri, C</creatorcontrib><creatorcontrib>Giusti, F</creatorcontrib><creatorcontrib>Lupetti, P</creatorcontrib><creatorcontrib>Giorgio, M</creatorcontrib><creatorcontrib>Pelicci, P G</creatorcontrib><creatorcontrib>Bernardi, P</creatorcontrib><creatorcontrib>Baldari, C T</creatorcontrib><title>p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca2+ homeostasis</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><description>p66Shc, a redox enzyme that enhances reactive oxygen species (ROS) production by mitochondria, promotes T cell apoptosis. We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca2+]c. p66Shc expression resulted in profound mitochondrial dysfunction in response to the Ca2+ ionophore A23187, as revealed by dissipation of mitochondrial transmembrane potential, cytochrome c release and decreased ATP levels. p66Shc expression also caused a dramatic alteration in the cells' Ca2+-handling ability, which resulted in Ca2+ overload after A23187 treatment. The impairment in Ca2+ homeostasis was ROS dependent and caused by defective Ca2+ extrusion due at least in part to decreased plasma membrane ATPase (PMCA) expression. Both effects of p66Shc required Ca2+-dependent serine-36 phosphorylation. The mitochondrial effects of p66Shc were potentiated by but not strictly dependent on the rise in [Ca2+]c. Thus, Ca2+-dependent p66Shc phosphorylation causes both mitochondrial dysfunction and impaired Ca2+ homeostasis, which synergize in promoting T cell apoptosis.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Calcimycin - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Cell death</subject><subject>Cytochrome</subject><subject>Down-Regulation - drug effects</subject><subject>Enzymes</subject><subject>Evolutionary biology</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Homeostasis</subject><subject>Homeostasis - drug effects</subject><subject>Humans</subject><subject>Jurkat Cells</subject><subject>Kinases</subject><subject>Lymphocytes</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - 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Academic</collection><jtitle>Cell death and differentiation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pellegrini, M</au><au>Finetti, F</au><au>Petronilli, V</au><au>Ulivieri, C</au><au>Giusti, F</au><au>Lupetti, P</au><au>Giorgio, M</au><au>Pelicci, P G</au><au>Bernardi, P</au><au>Baldari, C T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca2+ homeostasis</atitle><jtitle>Cell death and differentiation</jtitle><addtitle>Cell Death Differ</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>14</volume><issue>2</issue><spage>338</spage><epage>347</epage><pages>338-347</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>p66Shc, a redox enzyme that enhances reactive oxygen species (ROS) production by mitochondria, promotes T cell apoptosis. We have addressed the mechanisms regulating p66Shc-dependent apoptosis in T cells exposed to supraphysiological increases in [Ca2+]c. p66Shc expression resulted in profound mitochondrial dysfunction in response to the Ca2+ ionophore A23187, as revealed by dissipation of mitochondrial transmembrane potential, cytochrome c release and decreased ATP levels. p66Shc expression also caused a dramatic alteration in the cells' Ca2+-handling ability, which resulted in Ca2+ overload after A23187 treatment. The impairment in Ca2+ homeostasis was ROS dependent and caused by defective Ca2+ extrusion due at least in part to decreased plasma membrane ATPase (PMCA) expression. Both effects of p66Shc required Ca2+-dependent serine-36 phosphorylation. The mitochondrial effects of p66Shc were potentiated by but not strictly dependent on the rise in [Ca2+]c. Thus, Ca2+-dependent p66Shc phosphorylation causes both mitochondrial dysfunction and impaired Ca2+ homeostasis, which synergize in promoting T cell apoptosis.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>16794602</pmid><doi>10.1038/sj.cdd.4401997</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - metabolism Apoptosis Apoptosis - drug effects Calcimycin - pharmacology Calcium - metabolism Cell death Cytochrome Down-Regulation - drug effects Enzymes Evolutionary biology Flow Cytometry Gene Expression Regulation, Enzymologic - drug effects Homeostasis Homeostasis - drug effects Humans Jurkat Cells Kinases Lymphocytes Membrane Potential, Mitochondrial - drug effects Mitochondria Mitochondria - drug effects Mitochondria - enzymology Mitochondria - metabolism Oncology Oxidative stress Permeability Phosphorylation Phosphoserine - metabolism Plasma Plasma Membrane Calcium-Transporting ATPases - genetics Reactive Oxygen Species - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Shc Signaling Adaptor Proteins Src Homology 2 Domain-Containing, Transforming Protein 1 T-Lymphocytes - cytology T-Lymphocytes - drug effects T-Lymphocytes - immunology T-Lymphocytes - ultrastructure |
| title | p66SHC promotes T cell apoptosis by inducing mitochondrial dysfunction and impaired Ca2+ homeostasis |
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