Impact of endogenous nitric oxide on microglial cell energy metabolism and labile iron pool
Microglial activation is common in several neurodegenerative disorders. In the present study, we used the murine BV‐2 microglial cell line stimulated with γ‐interferon and lipopolysaccharide to gain new insights into the effects of endogenously produced NO on mitochondrial respiratory capacity, iron...
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| Veröffentlicht in: | Journal of neurochemistry 2002-05, Vol.81 (3), p.615-623 |
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| description | Microglial activation is common in several neurodegenerative disorders. In the present study, we used the murine BV‐2 microglial cell line stimulated with γ‐interferon and lipopolysaccharide to gain new insights into the effects of endogenously produced NO on mitochondrial respiratory capacity, iron regulatory protein activity, and redox‐active iron level. Using polarographic measurement of respiration of both intact and digitonin‐permeabilized cells, and spectrophotometric determination of individual respiratory chain complex activity, we showed that in addition to the reversible inhibition of cytochrome‐c oxidase, long‐term endogenous NO production reduced complex‐I and complex‐II activities in an irreversible manner. As a consequence, the cellular ATP level was decreased in NO‐producing cells, whereas ATPase activity was unaffected. We show that NO up‐regulates RNA‐binding of iron regulatory protein 1 in microglial cells, and strongly reduces the labile iron pool. Together these results point to a contribution of NO derived from inflammatory microglia to the misregulation of energy‐producing reactions and iron metabolism, often associated with the pathogenesis of neurodegenerative disorders. |
| doi_str_mv | 10.1046/j.1471-4159.2002.00864.x |
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In the present study, we used the murine BV‐2 microglial cell line stimulated with γ‐interferon and lipopolysaccharide to gain new insights into the effects of endogenously produced NO on mitochondrial respiratory capacity, iron regulatory protein activity, and redox‐active iron level. Using polarographic measurement of respiration of both intact and digitonin‐permeabilized cells, and spectrophotometric determination of individual respiratory chain complex activity, we showed that in addition to the reversible inhibition of cytochrome‐c oxidase, long‐term endogenous NO production reduced complex‐I and complex‐II activities in an irreversible manner. As a consequence, the cellular ATP level was decreased in NO‐producing cells, whereas ATPase activity was unaffected. We show that NO up‐regulates RNA‐binding of iron regulatory protein 1 in microglial cells, and strongly reduces the labile iron pool. Together these results point to a contribution of NO derived from inflammatory microglia to the misregulation of energy‐producing reactions and iron metabolism, often associated with the pathogenesis of neurodegenerative disorders.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.2002.00864.x</identifier><identifier>PMID: 12065670</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Aconitate Hydratase ; Aconitate Hydratase - antagonists & inhibitors ; Aconitate Hydratase - metabolism ; Adenosine Triphosphate ; Adenosine Triphosphate - metabolism ; Animals ; Biochemistry, Molecular Biology ; Biological and medical sciences ; Cell Line ; Cell Respiration ; Cell Respiration - drug effects ; Cytochrome c Group ; Cytochrome c Group - metabolism ; Electron Transport ; Electron Transport - physiology ; Electron Transport Complex I ; Electron Transport Complex II ; Energy Metabolism ; Energy Metabolism - drug effects ; Energy Metabolism - physiology ; Enzyme Activation ; Enzyme Activation - drug effects ; Fundamental and applied biological sciences. Psychology ; Interferon-gamma ; Interferon-gamma - pharmacology ; Intracellular Fluid ; Intracellular Fluid - metabolism ; Iron ; Iron - metabolism ; Iron-Regulatory Proteins ; Iron-Sulfur Proteins ; Iron-Sulfur Proteins - metabolism ; Isolated neuron and nerve. Neuroglia ; labile iron pool ; Life Sciences ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Mice ; Microglia ; Microglia - cytology ; Microglia - drug effects ; Microglia - metabolism ; microglial cells ; Multienzyme Complexes ; Multienzyme Complexes - antagonists & inhibitors ; Multienzyme Complexes - metabolism ; NADH, NADPH Oxidoreductases ; NADH, NADPH Oxidoreductases - antagonists & inhibitors ; NADH, NADPH Oxidoreductases - metabolism ; neurodegenerative diseases ; Nitric Oxide ; Nitric Oxide - metabolism ; Nitric Oxide - pharmacology ; Oxidoreductases ; Oxidoreductases - antagonists & inhibitors ; Oxidoreductases - metabolism ; Protein Binding ; Protein Binding - physiology ; respiratory chain ; RNA ; RNA - metabolism ; RNA-Binding Proteins ; RNA-Binding Proteins - metabolism ; Succinate Dehydrogenase ; Succinate Dehydrogenase - antagonists & inhibitors ; Succinate Dehydrogenase - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of neurochemistry, 2002-05, Vol.81 (3), p.615-623</ispartof><rights>2002 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5654-c962717bc838b7b2a2c0cfb366a996c4755f9db81caea49cd0898ce61dfde2a43</citedby><cites>FETCH-LOGICAL-c5654-c962717bc838b7b2a2c0cfb366a996c4755f9db81caea49cd0898ce61dfde2a43</cites><orcidid>0000-0003-2441-1966 ; 0000-0003-1959-7807</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.2002.00864.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.2002.00864.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13657861$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12065670$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00422911$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Chénais, Benoît</creatorcontrib><creatorcontrib>Morjani, Hamid</creatorcontrib><creatorcontrib>Drapier, Jean‐Claude</creatorcontrib><title>Impact of endogenous nitric oxide on microglial cell energy metabolism and labile iron pool</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Microglial activation is common in several neurodegenerative disorders. In the present study, we used the murine BV‐2 microglial cell line stimulated with γ‐interferon and lipopolysaccharide to gain new insights into the effects of endogenously produced NO on mitochondrial respiratory capacity, iron regulatory protein activity, and redox‐active iron level. Using polarographic measurement of respiration of both intact and digitonin‐permeabilized cells, and spectrophotometric determination of individual respiratory chain complex activity, we showed that in addition to the reversible inhibition of cytochrome‐c oxidase, long‐term endogenous NO production reduced complex‐I and complex‐II activities in an irreversible manner. As a consequence, the cellular ATP level was decreased in NO‐producing cells, whereas ATPase activity was unaffected. We show that NO up‐regulates RNA‐binding of iron regulatory protein 1 in microglial cells, and strongly reduces the labile iron pool. Together these results point to a contribution of NO derived from inflammatory microglia to the misregulation of energy‐producing reactions and iron metabolism, often associated with the pathogenesis of neurodegenerative disorders.</description><subject>Aconitate Hydratase</subject><subject>Aconitate Hydratase - antagonists & inhibitors</subject><subject>Aconitate Hydratase - metabolism</subject><subject>Adenosine Triphosphate</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Biochemistry, Molecular Biology</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell Respiration</subject><subject>Cell Respiration - drug effects</subject><subject>Cytochrome c Group</subject><subject>Cytochrome c Group - metabolism</subject><subject>Electron Transport</subject><subject>Electron Transport - physiology</subject><subject>Electron Transport Complex I</subject><subject>Electron Transport Complex II</subject><subject>Energy Metabolism</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy Metabolism - physiology</subject><subject>Enzyme Activation</subject><subject>Enzyme Activation - drug effects</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Interferon-gamma</subject><subject>Interferon-gamma - pharmacology</subject><subject>Intracellular Fluid</subject><subject>Intracellular Fluid - metabolism</subject><subject>Iron</subject><subject>Iron - metabolism</subject><subject>Iron-Regulatory Proteins</subject><subject>Iron-Sulfur Proteins</subject><subject>Iron-Sulfur Proteins - metabolism</subject><subject>Isolated neuron and nerve. Neuroglia</subject><subject>labile iron pool</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Mice</subject><subject>Microglia</subject><subject>Microglia - cytology</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>microglial cells</subject><subject>Multienzyme Complexes</subject><subject>Multienzyme Complexes - antagonists & inhibitors</subject><subject>Multienzyme Complexes - metabolism</subject><subject>NADH, NADPH Oxidoreductases</subject><subject>NADH, NADPH Oxidoreductases - antagonists & inhibitors</subject><subject>NADH, NADPH Oxidoreductases - metabolism</subject><subject>neurodegenerative diseases</subject><subject>Nitric Oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide - pharmacology</subject><subject>Oxidoreductases</subject><subject>Oxidoreductases - antagonists & inhibitors</subject><subject>Oxidoreductases - metabolism</subject><subject>Protein Binding</subject><subject>Protein Binding - physiology</subject><subject>respiratory chain</subject><subject>RNA</subject><subject>RNA - metabolism</subject><subject>RNA-Binding Proteins</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Succinate Dehydrogenase</subject><subject>Succinate Dehydrogenase - antagonists & inhibitors</subject><subject>Succinate Dehydrogenase - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUFv1DAQhS0EotvCX0C-gMQhweM4jnMAqVpRWrSCC5w4WI7jbL1y4sXOlt1_j82uWuACJ1ue741n3kMIAymBMP5mUwJroGBQtyUlhJaECM7K_SO0uC88RotUoUVFGD1D5zFuCAHOODxFZ0AJr3lDFujbzbhVesZ-wGbq_dpMfhfxZOdgNfZ72xvsJzxaHfzaWeWwNs4l1IT1AY9mVp13No5YTT12qrPOYBuSYuu9e4aeDMpF8_x0XqCvV--_LK-L1ecPN8vLVaFrXrNCt5w20HRaVKJrOqqoJnroKs5V23LNmroe2r4ToJVRrNU9Ea3QhkM_9IYqVl2gd8e-2103ml6baQ7KyW2wowoH6ZWVf1YmeyvX_k5SAZyS3OD1scHtX7Lry5XMbyR5SFuAO0jsq9NnwX_fmTjL0cZsippMsk42ICgFVv8TBMFII4AkUBzB5HGMwQz3IwCROW65kTlVmVOVOW75K265T9IXv2_-IDzlm4CXJ0BFrdwQ1KRtfOAqXjeC563eHrkfKcHDfw8gP35a5lv1E5iDxvM</recordid><startdate>200205</startdate><enddate>200205</enddate><creator>Chénais, Benoît</creator><creator>Morjani, Hamid</creator><creator>Drapier, Jean‐Claude</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Wiley</general><general>Blackwell Science</general><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>7TK</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2441-1966</orcidid><orcidid>https://orcid.org/0000-0003-1959-7807</orcidid></search><sort><creationdate>200205</creationdate><title>Impact of endogenous nitric oxide on microglial cell energy metabolism and labile iron pool</title><author>Chénais, Benoît ; Morjani, Hamid ; Drapier, Jean‐Claude</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5654-c962717bc838b7b2a2c0cfb366a996c4755f9db81caea49cd0898ce61dfde2a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aconitate Hydratase</topic><topic>Aconitate Hydratase - antagonists & inhibitors</topic><topic>Aconitate Hydratase - metabolism</topic><topic>Adenosine Triphosphate</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Biochemistry, Molecular Biology</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cell Respiration</topic><topic>Cell Respiration - drug effects</topic><topic>Cytochrome c Group</topic><topic>Cytochrome c Group - metabolism</topic><topic>Electron Transport</topic><topic>Electron Transport - physiology</topic><topic>Electron Transport Complex I</topic><topic>Electron Transport Complex II</topic><topic>Energy Metabolism</topic><topic>Energy Metabolism - drug effects</topic><topic>Energy Metabolism - physiology</topic><topic>Enzyme Activation</topic><topic>Enzyme Activation - drug effects</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Interferon-gamma</topic><topic>Interferon-gamma - pharmacology</topic><topic>Intracellular Fluid</topic><topic>Intracellular Fluid - metabolism</topic><topic>Iron</topic><topic>Iron - metabolism</topic><topic>Iron-Regulatory Proteins</topic><topic>Iron-Sulfur Proteins</topic><topic>Iron-Sulfur Proteins - metabolism</topic><topic>Isolated neuron and nerve. Neuroglia</topic><topic>labile iron pool</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Mice</topic><topic>Microglia</topic><topic>Microglia - cytology</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>microglial cells</topic><topic>Multienzyme Complexes</topic><topic>Multienzyme Complexes - antagonists & inhibitors</topic><topic>Multienzyme Complexes - metabolism</topic><topic>NADH, NADPH Oxidoreductases</topic><topic>NADH, NADPH Oxidoreductases - antagonists & inhibitors</topic><topic>NADH, NADPH Oxidoreductases - metabolism</topic><topic>neurodegenerative diseases</topic><topic>Nitric Oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide - pharmacology</topic><topic>Oxidoreductases</topic><topic>Oxidoreductases - antagonists & inhibitors</topic><topic>Oxidoreductases - metabolism</topic><topic>Protein Binding</topic><topic>Protein Binding - physiology</topic><topic>respiratory chain</topic><topic>RNA</topic><topic>RNA - metabolism</topic><topic>RNA-Binding Proteins</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Succinate Dehydrogenase</topic><topic>Succinate Dehydrogenase - antagonists & inhibitors</topic><topic>Succinate Dehydrogenase - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chénais, Benoît</creatorcontrib><creatorcontrib>Morjani, Hamid</creatorcontrib><creatorcontrib>Drapier, Jean‐Claude</creatorcontrib><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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chénais, Benoît</au><au>Morjani, Hamid</au><au>Drapier, Jean‐Claude</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of endogenous nitric oxide on microglial cell energy metabolism and labile iron pool</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2002-05</date><risdate>2002</risdate><volume>81</volume><issue>3</issue><spage>615</spage><epage>623</epage><pages>615-623</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Microglial activation is common in several neurodegenerative disorders. In the present study, we used the murine BV‐2 microglial cell line stimulated with γ‐interferon and lipopolysaccharide to gain new insights into the effects of endogenously produced NO on mitochondrial respiratory capacity, iron regulatory protein activity, and redox‐active iron level. Using polarographic measurement of respiration of both intact and digitonin‐permeabilized cells, and spectrophotometric determination of individual respiratory chain complex activity, we showed that in addition to the reversible inhibition of cytochrome‐c oxidase, long‐term endogenous NO production reduced complex‐I and complex‐II activities in an irreversible manner. As a consequence, the cellular ATP level was decreased in NO‐producing cells, whereas ATPase activity was unaffected. We show that NO up‐regulates RNA‐binding of iron regulatory protein 1 in microglial cells, and strongly reduces the labile iron pool. Together these results point to a contribution of NO derived from inflammatory microglia to the misregulation of energy‐producing reactions and iron metabolism, often associated with the pathogenesis of neurodegenerative disorders.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12065670</pmid><doi>10.1046/j.1471-4159.2002.00864.x</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-2441-1966</orcidid><orcidid>https://orcid.org/0000-0003-1959-7807</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aconitate Hydratase Aconitate Hydratase - antagonists & inhibitors Aconitate Hydratase - metabolism Adenosine Triphosphate Adenosine Triphosphate - metabolism Animals Biochemistry, Molecular Biology Biological and medical sciences Cell Line Cell Respiration Cell Respiration - drug effects Cytochrome c Group Cytochrome c Group - metabolism Electron Transport Electron Transport - physiology Electron Transport Complex I Electron Transport Complex II Energy Metabolism Energy Metabolism - drug effects Energy Metabolism - physiology Enzyme Activation Enzyme Activation - drug effects Fundamental and applied biological sciences. Psychology Interferon-gamma Interferon-gamma - pharmacology Intracellular Fluid Intracellular Fluid - metabolism Iron Iron - metabolism Iron-Regulatory Proteins Iron-Sulfur Proteins Iron-Sulfur Proteins - metabolism Isolated neuron and nerve. Neuroglia labile iron pool Life Sciences Lipopolysaccharides Lipopolysaccharides - pharmacology Mice Microglia Microglia - cytology Microglia - drug effects Microglia - metabolism microglial cells Multienzyme Complexes Multienzyme Complexes - antagonists & inhibitors Multienzyme Complexes - metabolism NADH, NADPH Oxidoreductases NADH, NADPH Oxidoreductases - antagonists & inhibitors NADH, NADPH Oxidoreductases - metabolism neurodegenerative diseases Nitric Oxide Nitric Oxide - metabolism Nitric Oxide - pharmacology Oxidoreductases Oxidoreductases - antagonists & inhibitors Oxidoreductases - metabolism Protein Binding Protein Binding - physiology respiratory chain RNA RNA - metabolism RNA-Binding Proteins RNA-Binding Proteins - metabolism Succinate Dehydrogenase Succinate Dehydrogenase - antagonists & inhibitors Succinate Dehydrogenase - metabolism Vertebrates: nervous system and sense organs |
| title | Impact of endogenous nitric oxide on microglial cell energy metabolism and labile iron pool |
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