Induction of peroxiredoxin I gene expression by LPS involves the Src/PI3K/JNK signalling pathway
Peroxiredoxin I (Prx I) belongs to a family of proteins with thiol-dependent peroxidase activity and is involved in the cellular protection against oxidative stress, the modulation of intracellular signalling cascades as well as the regulation of cell proliferation and apoptosis. In RAW 264.7 mouse...
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| Veröffentlicht in: | Biochimica et biophysica acta 2010-05, Vol.1799 (5), p.402-410 |
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| creator | Bast, Antje Fischer, Katja Erttmann, Saskia F. Walther, Reinhard |
| description | Peroxiredoxin I (Prx I) belongs to a family of proteins with thiol-dependent peroxidase activity and is involved in the cellular protection against oxidative stress, the modulation of intracellular signalling cascades as well as the regulation of cell proliferation and apoptosis. In RAW 264.7 mouse macrophage cells Prx I was up-regulated on the mRNA and protein level by lipopolysaccharide (LPS). Treatment of cells with LPS increased the phosphorylation of c-Jun-NH
2 terminal kinase (JNK) and protein kinase B (PKB). Both SP600125, an inhibitor of JNK, and LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), dose-dependently decreased LPS-induced Prx I mRNA expression. Furthermore, up-regulation of Prx I mRNA by LPS was diminished by the Src tyrosine kinase inhibitor PP2 and the iNOS inhibitor L-NMMA. LPS-dependent induction of Prx I is likely mediated by an activator protein-1 site within the Prx I promoter region binding JunB and c-Fos. In contrast, NFκB was not involved in the activation of Prx I transcription. Our results suggest that the up-regulation of Prx I gene expression by LPS is part of the cellular response to stress and may protect against oxidative stress-related injury in RAW 264.7 cells. |
| doi_str_mv | 10.1016/j.bbagrm.2009.11.015 |
| format | Article |
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2 terminal kinase (JNK) and protein kinase B (PKB). Both SP600125, an inhibitor of JNK, and LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), dose-dependently decreased LPS-induced Prx I mRNA expression. Furthermore, up-regulation of Prx I mRNA by LPS was diminished by the Src tyrosine kinase inhibitor PP2 and the iNOS inhibitor L-NMMA. LPS-dependent induction of Prx I is likely mediated by an activator protein-1 site within the Prx I promoter region binding JunB and c-Fos. In contrast, NFκB was not involved in the activation of Prx I transcription. Our results suggest that the up-regulation of Prx I gene expression by LPS is part of the cellular response to stress and may protect against oxidative stress-related injury in RAW 264.7 cells.</description><identifier>ISSN: 1874-9399</identifier><identifier>ISSN: 0006-3002</identifier><identifier>EISSN: 1876-4320</identifier><identifier>DOI: 10.1016/j.bbagrm.2009.11.015</identifier><identifier>PMID: 19941984</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; AP-1 ; Base Sequence ; Binding, Competitive ; Cell Line ; DNA Primers - genetics ; JNK ; JNK Mitogen-Activated Protein Kinases - metabolism ; Lipopolysaccharides - pharmacology ; Macrophage ; Macrophages - drug effects ; Macrophages - metabolism ; MAP Kinase Signaling System - drug effects ; Mice ; NF-kappa B - metabolism ; Nitric Oxide Synthase Type II - metabolism ; Oxidative Stress ; Peroxiredoxin ; Peroxiredoxins - genetics ; Peroxiredoxins - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K ; Proto-Oncogene Proteins c-akt - metabolism ; Proto-Oncogene Proteins c-fos - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Src ; src-Family Kinases - metabolism ; Transcription Factor AP-1 - metabolism ; Up-Regulation - drug effects</subject><ispartof>Biochimica et biophysica acta, 2010-05, Vol.1799 (5), p.402-410</ispartof><rights>2009 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-504d65be93cf03ce3f62ac700a8325fa6ecffeef34e40d545ebdb3ee81bb849c3</citedby><cites>FETCH-LOGICAL-c393t-504d65be93cf03ce3f62ac700a8325fa6ecffeef34e40d545ebdb3ee81bb849c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbagrm.2009.11.015$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19941984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bast, Antje</creatorcontrib><creatorcontrib>Fischer, Katja</creatorcontrib><creatorcontrib>Erttmann, Saskia F.</creatorcontrib><creatorcontrib>Walther, Reinhard</creatorcontrib><title>Induction of peroxiredoxin I gene expression by LPS involves the Src/PI3K/JNK signalling pathway</title><title>Biochimica et biophysica acta</title><addtitle>Biochim Biophys Acta</addtitle><description>Peroxiredoxin I (Prx I) belongs to a family of proteins with thiol-dependent peroxidase activity and is involved in the cellular protection against oxidative stress, the modulation of intracellular signalling cascades as well as the regulation of cell proliferation and apoptosis. In RAW 264.7 mouse macrophage cells Prx I was up-regulated on the mRNA and protein level by lipopolysaccharide (LPS). Treatment of cells with LPS increased the phosphorylation of c-Jun-NH
2 terminal kinase (JNK) and protein kinase B (PKB). Both SP600125, an inhibitor of JNK, and LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), dose-dependently decreased LPS-induced Prx I mRNA expression. Furthermore, up-regulation of Prx I mRNA by LPS was diminished by the Src tyrosine kinase inhibitor PP2 and the iNOS inhibitor L-NMMA. LPS-dependent induction of Prx I is likely mediated by an activator protein-1 site within the Prx I promoter region binding JunB and c-Fos. In contrast, NFκB was not involved in the activation of Prx I transcription. Our results suggest that the up-regulation of Prx I gene expression by LPS is part of the cellular response to stress and may protect against oxidative stress-related injury in RAW 264.7 cells.</description><subject>Animals</subject><subject>AP-1</subject><subject>Base Sequence</subject><subject>Binding, Competitive</subject><subject>Cell Line</subject><subject>DNA Primers - genetics</subject><subject>JNK</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophage</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Mice</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Oxidative Stress</subject><subject>Peroxiredoxin</subject><subject>Peroxiredoxins - genetics</subject><subject>Peroxiredoxins - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Src</subject><subject>src-Family Kinases - metabolism</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Up-Regulation - drug effects</subject><issn>1874-9399</issn><issn>0006-3002</issn><issn>1876-4320</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtPwzAQhC0E4v0PEPKNU1I7dtL4goQQj0IFSMDZ2M66uEqdYKeF_ntSWokbXHb38M2ONIPQCSUpJbQYTFOt1STM0owQkVKaEppvoX1aDouEs4xs_9w8EUyIPXQQ45SQgvbwLtqjQnAqSr6P3ka-mpvONR43FrcQmi8XoOqnxyM8AQ8YvtoAMa4QvcTjp2fs_KKpFxBx9w74OZjB04jdD-4e7nF0E6_q2vkJblX3_qmWR2jHqjrC8WYfotfrq5fL22T8eDO6vBgnhgnWJTnhVZFrEMxYwgwwW2TKDAlRJctyqwow1gJYxoGTKuc56EozgJJqXXJh2CE6W_9tQ_Mxh9jJmYsG6lp5aOZRDnkuGOei_J9kjJJhlmU9ydekCU2MAaxsg5upsJSUyFUJcirXJchVCZJS2ZfQy043BnM9g-pXtEm9B87XAPSBLBwEGY0Db6DqszedrBr3t8M3LPCavg</recordid><startdate>20100501</startdate><enddate>20100501</enddate><creator>Bast, Antje</creator><creator>Fischer, Katja</creator><creator>Erttmann, Saskia F.</creator><creator>Walther, Reinhard</creator><general>Elsevier 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>7X8</scope><scope>7T5</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20100501</creationdate><title>Induction of peroxiredoxin I gene expression by LPS involves the Src/PI3K/JNK signalling pathway</title><author>Bast, Antje ; Fischer, Katja ; Erttmann, Saskia F. ; Walther, Reinhard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-504d65be93cf03ce3f62ac700a8325fa6ecffeef34e40d545ebdb3ee81bb849c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>AP-1</topic><topic>Base Sequence</topic><topic>Binding, Competitive</topic><topic>Cell Line</topic><topic>DNA Primers - genetics</topic><topic>JNK</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophage</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Mice</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Oxidative Stress</topic><topic>Peroxiredoxin</topic><topic>Peroxiredoxins - genetics</topic><topic>Peroxiredoxins - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Src</topic><topic>src-Family Kinases - metabolism</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bast, Antje</creatorcontrib><creatorcontrib>Fischer, Katja</creatorcontrib><creatorcontrib>Erttmann, Saskia F.</creatorcontrib><creatorcontrib>Walther, Reinhard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Biochimica et biophysica acta</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bast, Antje</au><au>Fischer, Katja</au><au>Erttmann, Saskia F.</au><au>Walther, Reinhard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of peroxiredoxin I gene expression by LPS involves the Src/PI3K/JNK signalling pathway</atitle><jtitle>Biochimica et biophysica acta</jtitle><addtitle>Biochim Biophys Acta</addtitle><date>2010-05-01</date><risdate>2010</risdate><volume>1799</volume><issue>5</issue><spage>402</spage><epage>410</epage><pages>402-410</pages><issn>1874-9399</issn><issn>0006-3002</issn><eissn>1876-4320</eissn><abstract>Peroxiredoxin I (Prx I) belongs to a family of proteins with thiol-dependent peroxidase activity and is involved in the cellular protection against oxidative stress, the modulation of intracellular signalling cascades as well as the regulation of cell proliferation and apoptosis. In RAW 264.7 mouse macrophage cells Prx I was up-regulated on the mRNA and protein level by lipopolysaccharide (LPS). Treatment of cells with LPS increased the phosphorylation of c-Jun-NH
2 terminal kinase (JNK) and protein kinase B (PKB). Both SP600125, an inhibitor of JNK, and LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), dose-dependently decreased LPS-induced Prx I mRNA expression. Furthermore, up-regulation of Prx I mRNA by LPS was diminished by the Src tyrosine kinase inhibitor PP2 and the iNOS inhibitor L-NMMA. LPS-dependent induction of Prx I is likely mediated by an activator protein-1 site within the Prx I promoter region binding JunB and c-Fos. In contrast, NFκB was not involved in the activation of Prx I transcription. Our results suggest that the up-regulation of Prx I gene expression by LPS is part of the cellular response to stress and may protect against oxidative stress-related injury in RAW 264.7 cells.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>19941984</pmid><doi>10.1016/j.bbagrm.2009.11.015</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals AP-1 Base Sequence Binding, Competitive Cell Line DNA Primers - genetics JNK JNK Mitogen-Activated Protein Kinases - metabolism Lipopolysaccharides - pharmacology Macrophage Macrophages - drug effects Macrophages - metabolism MAP Kinase Signaling System - drug effects Mice NF-kappa B - metabolism Nitric Oxide Synthase Type II - metabolism Oxidative Stress Peroxiredoxin Peroxiredoxins - genetics Peroxiredoxins - metabolism Phosphatidylinositol 3-Kinases - metabolism PI3K Proto-Oncogene Proteins c-akt - metabolism Proto-Oncogene Proteins c-fos - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction - drug effects Src src-Family Kinases - metabolism Transcription Factor AP-1 - metabolism Up-Regulation - drug effects |
| title | Induction of peroxiredoxin I gene expression by LPS involves the Src/PI3K/JNK signalling pathway |
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