Reduction of Macrophage Activation after Antioxidant Enzymes Gene Transfer to Rat Insulinoma INS-1 Cells
Background. After transplantation, islet damage occurs through oxidative stress and host immune rejection mediated in part by macrophage activation. We investigated the influence of the overexpression of catalase (CAT) and Cu/Zn superoxide dismutase (Cu/Zn SOD) by rat insulinoma INS-1 beta cells exp...
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| Veröffentlicht in: | Immunobiology (1979) 2002-07, Vol.205 (3), p.193-203 |
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| creator | Karsten, Véronique Sigrist, Séverine Moriscot, Christine Benhamou, Pierre-Yves Lemarchand, Patricia Belcourt, Alain Poindron, Philippe Pinget, Michel Kessler, Laurence |
| description | Background. After transplantation, islet damage occurs through oxidative stress and host immune rejection mediated in part by macrophage activation. We investigated the influence of the overexpression of catalase (CAT) and Cu/Zn superoxide dismutase (Cu/Zn SOD) by rat insulinoma INS-1 beta cells exposed to oxidative stress on their viability and murine macrophage activation.
Methods. INS-1 cells were infected with adenoviral vectors containing CAT (AdCAT) or Cu/Zn SOD (AdSOD) genes. After 72 hours, noninfected and infected INS-1 cells were exposed to oxidative stress and their viability was assessed using a colorimetric assay. Murine peritoneal exudate macrophages (mPEM) incubated with the supernatant of infected and stressed INS-1 cells were tested for chemotaxis and cytokine release (TNF-a, IL-1b and IFN-g).
Results. After infection, AdCAT and AdSOD gene transfer protected INS-1 cells from the toxicity of different oxidative reagents. The exposure of noninfected INS-1 cells to oxidative stress stimulated mPEM chemotaxis. INS-1 cells infection with AdCAT or AdSOD reduced significantly mPEM chemotaxis from 2.41±0.31 to 1.61±0.17 and from 2.53±0.24 to 1.27±0.14 respectively (n=5; p |
| doi_str_mv | 10.1078/0171-2985-03471 |
| format | Article |
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Methods. INS-1 cells were infected with adenoviral vectors containing CAT (AdCAT) or Cu/Zn SOD (AdSOD) genes. After 72 hours, noninfected and infected INS-1 cells were exposed to oxidative stress and their viability was assessed using a colorimetric assay. Murine peritoneal exudate macrophages (mPEM) incubated with the supernatant of infected and stressed INS-1 cells were tested for chemotaxis and cytokine release (TNF-a, IL-1b and IFN-g).
Results. After infection, AdCAT and AdSOD gene transfer protected INS-1 cells from the toxicity of different oxidative reagents. The exposure of noninfected INS-1 cells to oxidative stress stimulated mPEM chemotaxis. INS-1 cells infection with AdCAT or AdSOD reduced significantly mPEM chemotaxis from 2.41±0.31 to 1.61±0.17 and from 2.53±0.24 to 1.27±0.14 respectively (n=5; p<0.05). Cytokine release by mPEM was stimulated after exposure to stressed noninfected INS-1 cell supernatant. CAT and Cu/Zn SOD overexpression by infected INS-1 cells decreased significantly the release of TNF-a from 268.18±30.18 to 81.40±23.58 pg/ml and from 446.96±75.47 to 20.37±2.38 pg/ml respectively (n=6; p<0.001). The overexpression of these enzymes also reduced significantly the release of IL-1b and IFN-g.
Conclusions. CAT or Cu/Zn SOD gene transfer to INS-1 cells preserved them from oxidative damage and reduced the macrophage activation induced by these pancreatic cells. Therefore, protection of pancreatic beta cells against oxidative injury by antioxidant enzymes gene transfer is an effective approach to overcome the deleterious actions of macrophages in pancreatic islet transplantation.</description><identifier>ISSN: 0171-2985</identifier><identifier>EISSN: 1878-3279</identifier><identifier>DOI: 10.1078/0171-2985-03471</identifier><identifier>PMID: 12182448</identifier><language>eng</language><publisher>Netherlands: Elsevier GmbH</publisher><subject>Animals ; Antioxidants - metabolism ; Catalase - biosynthesis ; Catalase - genetics ; Cells, Cultured ; Culture Media, Conditioned ; Cytokines - drug effects ; Cytokines - secretion ; Gene Expression Regulation, Enzymologic ; Gene Transfer Techniques ; Hydrogen Peroxide - pharmacology ; Insulinoma - enzymology ; Insulinoma - genetics ; Macrophage Activation - drug effects ; Macrophage Activation - physiology ; Macrophages, Peritoneal - drug effects ; Macrophages, Peritoneal - physiology ; Molsidomine - analogs & derivatives ; Molsidomine - pharmacology ; Oxidants - pharmacology ; Oxidative Stress - genetics ; Pancreatic Neoplasms - enzymology ; Pancreatic Neoplasms - genetics ; Rats ; Superoxide Dismutase - biosynthesis ; Superoxide Dismutase - genetics</subject><ispartof>Immunobiology (1979), 2002-07, Vol.205 (3), p.193-203</ispartof><rights>2002 Urban & Fischer Verlag</rights><rights>Copyright Urban & Fischer Verlag Jul 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-9b54c4c1aab956783529d496f2c3d9f7440942a25506e4a19692268096ef2dd03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/214023235?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976,64364,64366,64368,72218</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12182448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Karsten, Véronique</creatorcontrib><creatorcontrib>Sigrist, Séverine</creatorcontrib><creatorcontrib>Moriscot, Christine</creatorcontrib><creatorcontrib>Benhamou, Pierre-Yves</creatorcontrib><creatorcontrib>Lemarchand, Patricia</creatorcontrib><creatorcontrib>Belcourt, Alain</creatorcontrib><creatorcontrib>Poindron, Philippe</creatorcontrib><creatorcontrib>Pinget, Michel</creatorcontrib><creatorcontrib>Kessler, Laurence</creatorcontrib><title>Reduction of Macrophage Activation after Antioxidant Enzymes Gene Transfer to Rat Insulinoma INS-1 Cells</title><title>Immunobiology (1979)</title><addtitle>Immunobiology</addtitle><description>Background. After transplantation, islet damage occurs through oxidative stress and host immune rejection mediated in part by macrophage activation. We investigated the influence of the overexpression of catalase (CAT) and Cu/Zn superoxide dismutase (Cu/Zn SOD) by rat insulinoma INS-1 beta cells exposed to oxidative stress on their viability and murine macrophage activation.
Methods. INS-1 cells were infected with adenoviral vectors containing CAT (AdCAT) or Cu/Zn SOD (AdSOD) genes. After 72 hours, noninfected and infected INS-1 cells were exposed to oxidative stress and their viability was assessed using a colorimetric assay. Murine peritoneal exudate macrophages (mPEM) incubated with the supernatant of infected and stressed INS-1 cells were tested for chemotaxis and cytokine release (TNF-a, IL-1b and IFN-g).
Results. After infection, AdCAT and AdSOD gene transfer protected INS-1 cells from the toxicity of different oxidative reagents. The exposure of noninfected INS-1 cells to oxidative stress stimulated mPEM chemotaxis. INS-1 cells infection with AdCAT or AdSOD reduced significantly mPEM chemotaxis from 2.41±0.31 to 1.61±0.17 and from 2.53±0.24 to 1.27±0.14 respectively (n=5; p<0.05). Cytokine release by mPEM was stimulated after exposure to stressed noninfected INS-1 cell supernatant. CAT and Cu/Zn SOD overexpression by infected INS-1 cells decreased significantly the release of TNF-a from 268.18±30.18 to 81.40±23.58 pg/ml and from 446.96±75.47 to 20.37±2.38 pg/ml respectively (n=6; p<0.001). The overexpression of these enzymes also reduced significantly the release of IL-1b and IFN-g.
Conclusions. CAT or Cu/Zn SOD gene transfer to INS-1 cells preserved them from oxidative damage and reduced the macrophage activation induced by these pancreatic cells. Therefore, protection of pancreatic beta cells against oxidative injury by antioxidant enzymes gene transfer is an effective approach to overcome the deleterious actions of macrophages in pancreatic islet transplantation.</description><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Catalase - biosynthesis</subject><subject>Catalase - genetics</subject><subject>Cells, Cultured</subject><subject>Culture Media, Conditioned</subject><subject>Cytokines - drug effects</subject><subject>Cytokines - secretion</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Gene Transfer Techniques</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Insulinoma - enzymology</subject><subject>Insulinoma - genetics</subject><subject>Macrophage Activation - drug effects</subject><subject>Macrophage Activation - physiology</subject><subject>Macrophages, Peritoneal - drug effects</subject><subject>Macrophages, Peritoneal - physiology</subject><subject>Molsidomine - analogs & derivatives</subject><subject>Molsidomine - pharmacology</subject><subject>Oxidants - pharmacology</subject><subject>Oxidative Stress - genetics</subject><subject>Pancreatic Neoplasms - enzymology</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Rats</subject><subject>Superoxide Dismutase - biosynthesis</subject><subject>Superoxide Dismutase - genetics</subject><issn>0171-2985</issn><issn>1878-3279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kdFLHDEQh4NU9Gr77JuEPvRtayab3U0ej8Pqga1g7XPIJbM1cpucya7U_vXmvMNCoU9hMt_8GL4h5BTYF2CdPGfQQcWVbCpWiw4OyAxkJ6uad-odmb11j8n7nB8YA8U7eUSOgYPkQsgZub9FN9nRx0BjT78Zm-Lm3vxCOi-fT-a1YfoRE52HUvz2zoSRXoQ_zwNmeokB6V0yIfeFGCO9NSNdhjytfYiDocvvPyqgC1yv8wdy2Jt1xo_794T8_Hpxt7iqrm8ul4v5dWUFg7FSq0ZYYcGYlWraTtYNV06otue2dqrvhGBKcMObhrUoDKhWcd5KplrsuXOsPiGfd7mbFB8nzKMefLZlAxMwTlmDbFQrQBXw0z_gQ5xSKLtpDoLxmtdNgc53UPGSc8Jeb5IfTHrWwPT2AnrrWG8d69cLlImzfey0GtD95ffKC6B2ABYLTx6TztZjsOh8QjtqF_1_w18AameRNg</recordid><startdate>20020701</startdate><enddate>20020701</enddate><creator>Karsten, Véronique</creator><creator>Sigrist, Séverine</creator><creator>Moriscot, Christine</creator><creator>Benhamou, Pierre-Yves</creator><creator>Lemarchand, Patricia</creator><creator>Belcourt, Alain</creator><creator>Poindron, Philippe</creator><creator>Pinget, Michel</creator><creator>Kessler, Laurence</creator><general>Elsevier GmbH</general><general>Elsevier Science Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20020701</creationdate><title>Reduction of Macrophage Activation after Antioxidant Enzymes Gene Transfer to Rat Insulinoma INS-1 Cells</title><author>Karsten, Véronique ; Sigrist, Séverine ; Moriscot, Christine ; Benhamou, Pierre-Yves ; Lemarchand, Patricia ; Belcourt, Alain ; Poindron, Philippe ; Pinget, Michel ; Kessler, Laurence</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-9b54c4c1aab956783529d496f2c3d9f7440942a25506e4a19692268096ef2dd03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Catalase - biosynthesis</topic><topic>Catalase - genetics</topic><topic>Cells, Cultured</topic><topic>Culture Media, Conditioned</topic><topic>Cytokines - drug effects</topic><topic>Cytokines - secretion</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Gene Transfer Techniques</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Insulinoma - enzymology</topic><topic>Insulinoma - genetics</topic><topic>Macrophage Activation - drug effects</topic><topic>Macrophage Activation - physiology</topic><topic>Macrophages, Peritoneal - drug effects</topic><topic>Macrophages, Peritoneal - physiology</topic><topic>Molsidomine - analogs & derivatives</topic><topic>Molsidomine - pharmacology</topic><topic>Oxidants - pharmacology</topic><topic>Oxidative Stress - genetics</topic><topic>Pancreatic Neoplasms - enzymology</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Rats</topic><topic>Superoxide Dismutase - biosynthesis</topic><topic>Superoxide Dismutase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Karsten, Véronique</creatorcontrib><creatorcontrib>Sigrist, Séverine</creatorcontrib><creatorcontrib>Moriscot, Christine</creatorcontrib><creatorcontrib>Benhamou, Pierre-Yves</creatorcontrib><creatorcontrib>Lemarchand, Patricia</creatorcontrib><creatorcontrib>Belcourt, Alain</creatorcontrib><creatorcontrib>Poindron, Philippe</creatorcontrib><creatorcontrib>Pinget, Michel</creatorcontrib><creatorcontrib>Kessler, Laurence</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Immunobiology (1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Karsten, Véronique</au><au>Sigrist, Séverine</au><au>Moriscot, Christine</au><au>Benhamou, Pierre-Yves</au><au>Lemarchand, Patricia</au><au>Belcourt, Alain</au><au>Poindron, Philippe</au><au>Pinget, Michel</au><au>Kessler, Laurence</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction of Macrophage Activation after Antioxidant Enzymes Gene Transfer to Rat Insulinoma INS-1 Cells</atitle><jtitle>Immunobiology (1979)</jtitle><addtitle>Immunobiology</addtitle><date>2002-07-01</date><risdate>2002</risdate><volume>205</volume><issue>3</issue><spage>193</spage><epage>203</epage><pages>193-203</pages><issn>0171-2985</issn><eissn>1878-3279</eissn><abstract>Background. After transplantation, islet damage occurs through oxidative stress and host immune rejection mediated in part by macrophage activation. We investigated the influence of the overexpression of catalase (CAT) and Cu/Zn superoxide dismutase (Cu/Zn SOD) by rat insulinoma INS-1 beta cells exposed to oxidative stress on their viability and murine macrophage activation.
Methods. INS-1 cells were infected with adenoviral vectors containing CAT (AdCAT) or Cu/Zn SOD (AdSOD) genes. After 72 hours, noninfected and infected INS-1 cells were exposed to oxidative stress and their viability was assessed using a colorimetric assay. Murine peritoneal exudate macrophages (mPEM) incubated with the supernatant of infected and stressed INS-1 cells were tested for chemotaxis and cytokine release (TNF-a, IL-1b and IFN-g).
Results. After infection, AdCAT and AdSOD gene transfer protected INS-1 cells from the toxicity of different oxidative reagents. The exposure of noninfected INS-1 cells to oxidative stress stimulated mPEM chemotaxis. INS-1 cells infection with AdCAT or AdSOD reduced significantly mPEM chemotaxis from 2.41±0.31 to 1.61±0.17 and from 2.53±0.24 to 1.27±0.14 respectively (n=5; p<0.05). Cytokine release by mPEM was stimulated after exposure to stressed noninfected INS-1 cell supernatant. CAT and Cu/Zn SOD overexpression by infected INS-1 cells decreased significantly the release of TNF-a from 268.18±30.18 to 81.40±23.58 pg/ml and from 446.96±75.47 to 20.37±2.38 pg/ml respectively (n=6; p<0.001). The overexpression of these enzymes also reduced significantly the release of IL-1b and IFN-g.
Conclusions. CAT or Cu/Zn SOD gene transfer to INS-1 cells preserved them from oxidative damage and reduced the macrophage activation induced by these pancreatic cells. Therefore, protection of pancreatic beta cells against oxidative injury by antioxidant enzymes gene transfer is an effective approach to overcome the deleterious actions of macrophages in pancreatic islet transplantation.</abstract><cop>Netherlands</cop><pub>Elsevier GmbH</pub><pmid>12182448</pmid><doi>10.1078/0171-2985-03471</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Antioxidants - metabolism Catalase - biosynthesis Catalase - genetics Cells, Cultured Culture Media, Conditioned Cytokines - drug effects Cytokines - secretion Gene Expression Regulation, Enzymologic Gene Transfer Techniques Hydrogen Peroxide - pharmacology Insulinoma - enzymology Insulinoma - genetics Macrophage Activation - drug effects Macrophage Activation - physiology Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - physiology Molsidomine - analogs & derivatives Molsidomine - pharmacology Oxidants - pharmacology Oxidative Stress - genetics Pancreatic Neoplasms - enzymology Pancreatic Neoplasms - genetics Rats Superoxide Dismutase - biosynthesis Superoxide Dismutase - genetics |
| title | Reduction of Macrophage Activation after Antioxidant Enzymes Gene Transfer to Rat Insulinoma INS-1 Cells |
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