Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species
Microglia, major immune effector cells in the central nervous system, become activated during brain injury. In this study we showed that the blood component plasminogen/plasmin activates microglia. Plasminogen-induced IL-1beta, TNF-alpha, and iNOS mRNA expression in primary cultured rat microglia an...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2003-12, Vol.312 (4), p.969-974 |
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| creator | Min, Kyoung-jin Jou, Ilo Joe, Eunhye |
| description | Microglia, major immune effector cells in the central nervous system, become activated during brain injury. In this study we showed that the blood component plasminogen/plasmin activates microglia. Plasminogen-induced IL-1beta, TNF-alpha, and iNOS mRNA expression in primary cultured rat microglia and BV2 murine microglial cells. Plasmin caused a similar response. Serine protease inhibitors suppressed both plasminogen- and plasmin-induced IL-1beta and TNF-alpha expression, indicating the importance of serine protease activity in plasminogen/plasmin activation of microglia. Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells. Furthermore, plasminogen stimulated CREB and NF-kappaB DNA binding activity, and this activation was also reduced by trolox and NAC. These results suggest that plasminogen activates microglia via stimulation of ROS production. |
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In this study we showed that the blood component plasminogen/plasmin activates microglia. Plasminogen-induced IL-1beta, TNF-alpha, and iNOS mRNA expression in primary cultured rat microglia and BV2 murine microglial cells. Plasmin caused a similar response. Serine protease inhibitors suppressed both plasminogen- and plasmin-induced IL-1beta and TNF-alpha expression, indicating the importance of serine protease activity in plasminogen/plasmin activation of microglia. Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells. Furthermore, plasminogen stimulated CREB and NF-kappaB DNA binding activity, and this activation was also reduced by trolox and NAC. These results suggest that plasminogen activates microglia via stimulation of ROS production.</description><identifier>ISSN: 0006-291X</identifier><identifier>PMID: 14651966</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cell Line ; Cells, Cultured ; Dose-Response Relationship, Drug ; Fibrinolysin - metabolism ; Fibrinolysin - pharmacology ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; Homeostasis - drug effects ; Homeostasis - physiology ; Interleukin-1 - biosynthesis ; Mice ; Microglia - drug effects ; Microglia - metabolism ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase Type II ; Plasminogen - metabolism ; Plasminogen - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Biochemical and biophysical research communications, 2003-12, Vol.312 (4), p.969-974</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14651966$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Min, Kyoung-jin</creatorcontrib><creatorcontrib>Jou, Ilo</creatorcontrib><creatorcontrib>Joe, Eunhye</creatorcontrib><title>Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Microglia, major immune effector cells in the central nervous system, become activated during brain injury. In this study we showed that the blood component plasminogen/plasmin activates microglia. Plasminogen-induced IL-1beta, TNF-alpha, and iNOS mRNA expression in primary cultured rat microglia and BV2 murine microglial cells. Plasmin caused a similar response. Serine protease inhibitors suppressed both plasminogen- and plasmin-induced IL-1beta and TNF-alpha expression, indicating the importance of serine protease activity in plasminogen/plasmin activation of microglia. Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells. Furthermore, plasminogen stimulated CREB and NF-kappaB DNA binding activity, and this activation was also reduced by trolox and NAC. These results suggest that plasminogen activates microglia via stimulation of ROS production.</description><subject>Animals</subject><subject>Cell Line</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fibrinolysin - metabolism</subject><subject>Fibrinolysin - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>Homeostasis - drug effects</subject><subject>Homeostasis - physiology</subject><subject>Interleukin-1 - biosynthesis</subject><subject>Mice</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Plasminogen - metabolism</subject><subject>Plasminogen - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0006-291X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kMFOwzAQRH0A0VL4BeQTN0ve1EnqI6ooVKqAQw7coo29La4cJ8QJon-PEeU0Gs3b0Wgv2FxKWYhMw_uMXcd4lBJAFfqKzZLkoItizo5vHmPrQnegIFywkyHLtzsBDY3IMVhevWwE-v4DeT90KR9dF7gLvHVm6A7eIXeRD3SYPI7ptjklg4n6It59n1Itjz0ZR_GGXe7RR7o964JVm8dq_Sx2r0_b9cNO9LkqhMrtCsqlttJa02iljW1IWqkz1Jklq8pMmyIDVa4A94YMGLC5kmk35JnOlwt2_1eb5n5OFMe6ddGQ9xiom2JdggIN8AvencGpacnW_eBaHE71_3OWPxgaYLY</recordid><startdate>20031226</startdate><enddate>20031226</enddate><creator>Min, Kyoung-jin</creator><creator>Jou, Ilo</creator><creator>Joe, Eunhye</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20031226</creationdate><title>Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species</title><author>Min, Kyoung-jin ; Jou, Ilo ; Joe, Eunhye</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p546-45d81739d0ddcb949cdbe0d092a92ded4729c6214781afcec1c1d540ced152953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Cell Line</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fibrinolysin - metabolism</topic><topic>Fibrinolysin - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - physiology</topic><topic>Homeostasis - drug effects</topic><topic>Homeostasis - physiology</topic><topic>Interleukin-1 - biosynthesis</topic><topic>Mice</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Nitric Oxide Synthase - biosynthesis</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Plasminogen - metabolism</topic><topic>Plasminogen - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Min, Kyoung-jin</creatorcontrib><creatorcontrib>Jou, Ilo</creatorcontrib><creatorcontrib>Joe, Eunhye</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Min, Kyoung-jin</au><au>Jou, Ilo</au><au>Joe, Eunhye</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2003-12-26</date><risdate>2003</risdate><volume>312</volume><issue>4</issue><spage>969</spage><epage>974</epage><pages>969-974</pages><issn>0006-291X</issn><abstract>Microglia, major immune effector cells in the central nervous system, become activated during brain injury. In this study we showed that the blood component plasminogen/plasmin activates microglia. Plasminogen-induced IL-1beta, TNF-alpha, and iNOS mRNA expression in primary cultured rat microglia and BV2 murine microglial cells. Plasmin caused a similar response. Serine protease inhibitors suppressed both plasminogen- and plasmin-induced IL-1beta and TNF-alpha expression, indicating the importance of serine protease activity in plasminogen/plasmin activation of microglia. Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells. Furthermore, plasminogen stimulated CREB and NF-kappaB DNA binding activity, and this activation was also reduced by trolox and NAC. These results suggest that plasminogen activates microglia via stimulation of ROS production.</abstract><cop>United States</cop><pmid>14651966</pmid><tpages>6</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2003-12, Vol.312 (4), p.969-974 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Cell Line Cells, Cultured Dose-Response Relationship, Drug Fibrinolysin - metabolism Fibrinolysin - pharmacology Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Homeostasis - drug effects Homeostasis - physiology Interleukin-1 - biosynthesis Mice Microglia - drug effects Microglia - metabolism Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase Type II Plasminogen - metabolism Plasminogen - pharmacology Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Tumor Necrosis Factor-alpha - biosynthesis |
| title | Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species |
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