Peroxynitrite Activates the NLRP3 Inflammasome Cascade in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis
Neuroinflammation, characterized by the appearance of reactive microglial and astroglial cells, is one of the several pathogenic mechanisms of amyotrophic lateral sclerosis (ALS), a fast-progressing and fatal neurodegenerative disease. Cerebrospinal fluid and spinal cord of ALS patients and SOD1 mut...
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| Veröffentlicht in: | Molecular neurobiology 2018-03, Vol.55 (3), p.2350-2361 |
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| creator | Bellezza, Ilaria Grottelli, Silvia Costanzi, Egidia Scarpelli, Paolo Pigna, Eva Morozzi, Giulio Mezzasoma, Letizia Peirce, Matthew J. Moresi, Viviana Adamo, Sergio Minelli, Alba |
| description | Neuroinflammation, characterized by the appearance of reactive microglial and astroglial cells, is one of the several pathogenic mechanisms of amyotrophic lateral sclerosis (ALS), a fast-progressing and fatal neurodegenerative disease. Cerebrospinal fluid and spinal cord of ALS patients and SOD1 mutant mice show high concentrations of IL-1β. This interleukin, expressed as an inactive precursor, undergoes a proteolytic maturation by caspase1, whose activation, in turn, depends on inflammasomes. Whether and how inflammasome is activated in ALS models is still to be clarified. The mechanism of inflammasome activation was studied in murine microglial cells overexpressing hSOD1(G93A) and verified in the spinal cord of hSOD1(G93A) mice. Murine microglial hSOD1(G93A) cells express all the inflammasome components and LPS activates caspase1 leading to an increase in the secretion of IL-1β. By activating NF-κB, LPS increases ROS and NO levels that spontaneously react to form peroxynitrite, thus leading to protein nitration. Reduction in peroxynitrite levels results in a decrease in caspase1 activity. Protein nitration and caspase1 activity are concomitantly increased in the spinal cord of pre-symptomatic SOD1(G93A) mice. Oxidative/nitrosative stress induces peroxynitrite formation that may be a key trigger of caspase1/inflammasome activation. Peroxynitrite formation may play a critical role in inflammasome activation and might be exploited as potential therapeutic target for ALS. |
| doi_str_mv | 10.1007/s12035-017-0502-x |
| format | Article |
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Cerebrospinal fluid and spinal cord of ALS patients and SOD1 mutant mice show high concentrations of IL-1β. This interleukin, expressed as an inactive precursor, undergoes a proteolytic maturation by caspase1, whose activation, in turn, depends on inflammasomes. Whether and how inflammasome is activated in ALS models is still to be clarified. The mechanism of inflammasome activation was studied in murine microglial cells overexpressing hSOD1(G93A) and verified in the spinal cord of hSOD1(G93A) mice. Murine microglial hSOD1(G93A) cells express all the inflammasome components and LPS activates caspase1 leading to an increase in the secretion of IL-1β. By activating NF-κB, LPS increases ROS and NO levels that spontaneously react to form peroxynitrite, thus leading to protein nitration. Reduction in peroxynitrite levels results in a decrease in caspase1 activity. Protein nitration and caspase1 activity are concomitantly increased in the spinal cord of pre-symptomatic SOD1(G93A) mice. Oxidative/nitrosative stress induces peroxynitrite formation that may be a key trigger of caspase1/inflammasome activation. Peroxynitrite formation may play a critical role in inflammasome activation and might be exploited as potential therapeutic target for ALS.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0502-x</identifier><identifier>PMID: 28357805</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - genetics ; Amyotrophic Lateral Sclerosis - metabolism ; Animal models ; Animals ; Astrocytes ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line, Transformed ; Cerebrospinal fluid ; Disease Models, Animal ; Female ; IL-1β ; Inflammasomes ; Inflammation ; Lipopolysaccharides ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglial cells ; Neurobiology ; Neurology ; Neurosciences ; NF-κB protein ; Nitration ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Peroxynitrite ; Peroxynitrous Acid - metabolism ; Proteolysis ; Reactive oxygen species ; Rodents ; Spinal cord ; Superoxide dismutase ; Superoxide Dismutase-1 - genetics ; Superoxide Dismutase-1 - metabolism ; Therapeutic applications</subject><ispartof>Molecular neurobiology, 2018-03, Vol.55 (3), p.2350-2361</ispartof><rights>Springer Science+Business Media New York 2017</rights><rights>Molecular Neurobiology is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-e28dd9579cf204c6bf0501f0e42eb3e5e3e3a5e8e56fc697c92c7640fcc0edfa3</citedby><cites>FETCH-LOGICAL-c415t-e28dd9579cf204c6bf0501f0e42eb3e5e3e3a5e8e56fc697c92c7640fcc0edfa3</cites><orcidid>0000-0002-8106-1600</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-017-0502-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0502-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28357805$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bellezza, Ilaria</creatorcontrib><creatorcontrib>Grottelli, Silvia</creatorcontrib><creatorcontrib>Costanzi, Egidia</creatorcontrib><creatorcontrib>Scarpelli, Paolo</creatorcontrib><creatorcontrib>Pigna, Eva</creatorcontrib><creatorcontrib>Morozzi, Giulio</creatorcontrib><creatorcontrib>Mezzasoma, Letizia</creatorcontrib><creatorcontrib>Peirce, Matthew J.</creatorcontrib><creatorcontrib>Moresi, Viviana</creatorcontrib><creatorcontrib>Adamo, Sergio</creatorcontrib><creatorcontrib>Minelli, Alba</creatorcontrib><title>Peroxynitrite Activates the NLRP3 Inflammasome Cascade in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Neuroinflammation, characterized by the appearance of reactive microglial and astroglial cells, is one of the several pathogenic mechanisms of amyotrophic lateral sclerosis (ALS), a fast-progressing and fatal neurodegenerative disease. Cerebrospinal fluid and spinal cord of ALS patients and SOD1 mutant mice show high concentrations of IL-1β. This interleukin, expressed as an inactive precursor, undergoes a proteolytic maturation by caspase1, whose activation, in turn, depends on inflammasomes. Whether and how inflammasome is activated in ALS models is still to be clarified. The mechanism of inflammasome activation was studied in murine microglial cells overexpressing hSOD1(G93A) and verified in the spinal cord of hSOD1(G93A) mice. Murine microglial hSOD1(G93A) cells express all the inflammasome components and LPS activates caspase1 leading to an increase in the secretion of IL-1β. By activating NF-κB, LPS increases ROS and NO levels that spontaneously react to form peroxynitrite, thus leading to protein nitration. Reduction in peroxynitrite levels results in a decrease in caspase1 activity. Protein nitration and caspase1 activity are concomitantly increased in the spinal cord of pre-symptomatic SOD1(G93A) mice. Oxidative/nitrosative stress induces peroxynitrite formation that may be a key trigger of caspase1/inflammasome activation. Peroxynitrite formation may play a critical role in inflammasome activation and might be exploited as potential therapeutic target for ALS.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Animal models</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Line, Transformed</subject><subject>Cerebrospinal fluid</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>IL-1β</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Lipopolysaccharides</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microglial cells</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>NF-κB protein</subject><subject>Nitration</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Peroxynitrite</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Proteolysis</subject><subject>Reactive oxygen species</subject><subject>Rodents</subject><subject>Spinal cord</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase-1 - genetics</subject><subject>Superoxide Dismutase-1 - metabolism</subject><subject>Therapeutic applications</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU1vEzEQhi1ERUPhB3BBlriUw5YZe71rH6MApVJKK9qeLcc7plvtR2pvUPLvcZV-SEhcZg7zzDvz6mXsA8IJAtRfEgqQqgCsC1Agiu0rNkOlTIGoxWs2A21kUVelPmRvU7oDEAKhfsMOhZaq1qBm7P6S4rjdDe0U24n43E_tHzdR4tMt8Z_LX5eSnw2hc33v0tgTX7jkXUO8HfjVxVc8PjVy_pmfj5tEuTbU8THweb8bpziub1vPl1ktuo5f-S5fSm16xw6C6xK9f-xH7Ob7t-vFj2J5cXq2mC8LX6KaChK6aYyqjQ8CSl-tQraIAagUtJKkSJJ0ijSpKvjK1N4In61C8B6oCU4eseO97jqO9xtKk-3b5Knr3ED5XYtai9LoUlcZ_fQPejdu4pC_swIQ0RgpRKZwT_nsI0UKdh3b3sWdRbAPedh9HjbnYR_ysNu88_FRebPqqXneeAogA2IPpDwaflN8Of1_1b_vDZVs</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Bellezza, Ilaria</creator><creator>Grottelli, Silvia</creator><creator>Costanzi, Egidia</creator><creator>Scarpelli, Paolo</creator><creator>Pigna, Eva</creator><creator>Morozzi, Giulio</creator><creator>Mezzasoma, Letizia</creator><creator>Peirce, Matthew J.</creator><creator>Moresi, Viviana</creator><creator>Adamo, Sergio</creator><creator>Minelli, Alba</creator><general>Springer US</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8106-1600</orcidid></search><sort><creationdate>20180301</creationdate><title>Peroxynitrite Activates the NLRP3 Inflammasome Cascade in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis</title><author>Bellezza, Ilaria ; Grottelli, Silvia ; Costanzi, Egidia ; Scarpelli, Paolo ; Pigna, Eva ; Morozzi, Giulio ; Mezzasoma, Letizia ; Peirce, Matthew J. ; Moresi, Viviana ; Adamo, Sergio ; Minelli, Alba</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-e28dd9579cf204c6bf0501f0e42eb3e5e3e3a5e8e56fc697c92c7640fcc0edfa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Animal models</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Line, Transformed</topic><topic>Cerebrospinal fluid</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>IL-1β</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Lipopolysaccharides</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Microglial cells</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>NF-κB protein</topic><topic>Nitration</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Peroxynitrite</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Proteolysis</topic><topic>Reactive oxygen species</topic><topic>Rodents</topic><topic>Spinal cord</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase-1 - 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Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bellezza, Ilaria</au><au>Grottelli, Silvia</au><au>Costanzi, Egidia</au><au>Scarpelli, Paolo</au><au>Pigna, Eva</au><au>Morozzi, Giulio</au><au>Mezzasoma, Letizia</au><au>Peirce, Matthew J.</au><au>Moresi, Viviana</au><au>Adamo, Sergio</au><au>Minelli, Alba</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxynitrite Activates the NLRP3 Inflammasome Cascade in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>55</volume><issue>3</issue><spage>2350</spage><epage>2361</epage><pages>2350-2361</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Neuroinflammation, characterized by the appearance of reactive microglial and astroglial cells, is one of the several pathogenic mechanisms of amyotrophic lateral sclerosis (ALS), a fast-progressing and fatal neurodegenerative disease. Cerebrospinal fluid and spinal cord of ALS patients and SOD1 mutant mice show high concentrations of IL-1β. This interleukin, expressed as an inactive precursor, undergoes a proteolytic maturation by caspase1, whose activation, in turn, depends on inflammasomes. Whether and how inflammasome is activated in ALS models is still to be clarified. The mechanism of inflammasome activation was studied in murine microglial cells overexpressing hSOD1(G93A) and verified in the spinal cord of hSOD1(G93A) mice. Murine microglial hSOD1(G93A) cells express all the inflammasome components and LPS activates caspase1 leading to an increase in the secretion of IL-1β. By activating NF-κB, LPS increases ROS and NO levels that spontaneously react to form peroxynitrite, thus leading to protein nitration. Reduction in peroxynitrite levels results in a decrease in caspase1 activity. Protein nitration and caspase1 activity are concomitantly increased in the spinal cord of pre-symptomatic SOD1(G93A) mice. Oxidative/nitrosative stress induces peroxynitrite formation that may be a key trigger of caspase1/inflammasome activation. Peroxynitrite formation may play a critical role in inflammasome activation and might be exploited as potential therapeutic target for ALS.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28357805</pmid><doi>10.1007/s12035-017-0502-x</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-8106-1600</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Animal models Animals Astrocytes Biomedical and Life Sciences Biomedicine Cell Biology Cell Line, Transformed Cerebrospinal fluid Disease Models, Animal Female IL-1β Inflammasomes Inflammation Lipopolysaccharides Mice Mice, Inbred C57BL Mice, Transgenic Microglial cells Neurobiology Neurology Neurosciences NF-κB protein Nitration NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Peroxynitrite Peroxynitrous Acid - metabolism Proteolysis Reactive oxygen species Rodents Spinal cord Superoxide dismutase Superoxide Dismutase-1 - genetics Superoxide Dismutase-1 - metabolism Therapeutic applications |
| title | Peroxynitrite Activates the NLRP3 Inflammasome Cascade in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis |
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