Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions
Identifieur interne : 001298 ( Istex/Corpus ); précédent : 001297; suivant : 001299Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions
Auteurs : Guo Yin ; Hyejin Jeon ; Shinrye Lee ; Ho Lee ; Je Cho ; Kyoungho SukSource :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2009-08-15.
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Abstract
Proteomic analysis of cerebrospinal fluid (CSF) samples derived from patients with Alzheimer's disease (AD) or Parkinson's disease (PD) was performed. On the basis of liquid chromatography–tandem mass spectrometry, two‐dimensional gel electrophoresis analysis, and Western blot validation, it was found that the level of soluble form of monocyte differentiation antigen CD14 precursor was elevated in CSF from AD or PD patients compared with normal subjects. The soluble CD14 protein and mRNA expression was detected in microglia cells, indicating that microglia may be a cellular source of soluble CD14 in CSF. Next, the role of soluble CD14 in the regulation of glial functions was investigated. Soluble CD14 inhibited lipopolysaccharide (LPS)‐ or LPS/interferon‐gamma‐induced nitric oxide production and cell death of microglia and astrocytes. Soluble CD14 suppressed glial neurotoxicity in a coculture of glia/neuroblastoma. In addition, soluble CD14 moderately enhanced phagocytic activity of microglia. These results suggest that microglia‐derived soluble CD14 is a candidate CSF biomarker for AD and PD, and the soluble CD14 may inhibit glial activation by interfering with LPS effects. © 2009 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.22081
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ISTEX:6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49Le document en format XML
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Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-08-15">2009-08-15</date><biblScope unit="volume">87</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2578">2578</biblScope><biblScope unit="page" to="2590">2590</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49</idno><idno type="DOI">10.1002/jnr.22081</idno><idno type="ArticleID">JNR22081</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>cerebrospinal fluid (CSF)</term><term>glia</term><term>liquid chromatography–tandem mass spectrometry (LC‐MS/MS)</term><term>monocyte differentiation antigen CD14 precursor</term><term>neurodegenerative diseases</term><term>phagocytosis</term><term>two‐dimensional gel electrophoresis (2‐DE)</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Proteomic analysis of cerebrospinal fluid (CSF) samples derived from patients with Alzheimer's disease (AD) or Parkinson's disease (PD) was performed. On the basis of liquid chromatography–tandem mass spectrometry, two‐dimensional gel electrophoresis analysis, and Western blot validation, it was found that the level of soluble form of monocyte differentiation antigen CD14 precursor was elevated in CSF from AD or PD patients compared with normal subjects. The soluble CD14 protein and mRNA expression was detected in microglia cells, indicating that microglia may be a cellular source of soluble CD14 in CSF. Next, the role of soluble CD14 in the regulation of glial functions was investigated. Soluble CD14 inhibited lipopolysaccharide (LPS)‐ or LPS/interferon‐gamma‐induced nitric oxide production and cell death of microglia and astrocytes. Soluble CD14 suppressed glial neurotoxicity in a coculture of glia/neuroblastoma. In addition, soluble CD14 moderately enhanced phagocytic activity of microglia. These results suggest that microglia‐derived soluble CD14 is a candidate CSF biomarker for AD and PD, and the soluble CD14 may inhibit glial activation by interfering with LPS effects. © 2009 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Guo Nan Yin</name><affiliations><json:string>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</json:string></affiliations></json:item><json:item><name>Hyejin Jeon</name><affiliations><json:string>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</json:string></affiliations></json:item><json:item><name>Shinrye Lee</name><affiliations><json:string>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</json:string></affiliations></json:item><json:item><name>Ho Won Lee</name><affiliations><json:string>Department of Neurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Korea</json:string></affiliations></json:item><json:item><name>Je‐Yoel Cho</name><affiliations><json:string>Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Korea</json:string></affiliations></json:item><json:item><name>Kyoungho Suk</name><affiliations><json:string>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>neurodegenerative diseases</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cerebrospinal fluid (CSF)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>liquid chromatography–tandem mass spectrometry (LC‐MS/MS)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>monocyte differentiation antigen CD14 precursor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>two‐dimensional gel electrophoresis (2‐DE)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>phagocytosis</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Proteomic analysis of cerebrospinal fluid (CSF) samples derived from patients with Alzheimer's disease (AD) or Parkinson's disease (PD) was performed. On the basis of liquid chromatography–tandem mass spectrometry, two‐dimensional gel electrophoresis analysis, and Western blot validation, it was found that the level of soluble form of monocyte differentiation antigen CD14 precursor was elevated in CSF from AD or PD patients compared with normal subjects. The soluble CD14 protein and mRNA expression was detected in microglia cells, indicating that microglia may be a cellular source of soluble CD14 in CSF. Next, the role of soluble CD14 in the regulation of glial functions was investigated. Soluble CD14 inhibited lipopolysaccharide (LPS)‐ or LPS/interferon‐gamma‐induced nitric oxide production and cell death of microglia and astrocytes. Soluble CD14 suppressed glial neurotoxicity in a coculture of glia/neuroblastoma. In addition, soluble CD14 moderately enhanced phagocytic activity of microglia. These results suggest that microglia‐derived soluble CD14 is a candidate CSF biomarker for AD and PD, and the soluble CD14 may inhibit glial activation by interfering with LPS effects. © 2009 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.076</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1217</abstractCharCount><pdfWordCount>8467</pdfWordCount><pdfCharCount>52156</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>173</abstractWordCount></qualityIndicators><title>Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions</title><genre><json:string>article</json:string></genre><host><volume>87</volume><pages><total>13</total><last>2590</last><first>2578</first></pages><issn><json:string>0360-4012</json:string></issn><issue>11</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1097-4547</json:string></eissn><title>Journal of Neuroscience Research</title><doi><json:string>10.1002/(ISSN)1097-4547</json:string></doi></host><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/jnr.22081</json:string></doi><id>6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2009</date></publicationStmt><notesStmt><note>Basic Research Program of the Korea Science and Engineering Foundation - No. R01‐2006‐000‐10314‐0;</note><note>Bio R&D program through the Korea Science and Engineering Foundation</note><note>Ministry of Education, Science and Technology - No. 2008‐04090;</note><note>Korea Research Foundation</note><note>Korean Government (MOEHRD, Basic Research Promotion Fund) - No. KRF‐2006‐005‐J04202;</note><note>Brain Korea 21 Project</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions</title><author><persName><forename type="first">Guo Nan</forename><surname>Yin</surname></persName><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation></author><author><persName><forename type="first">Hyejin</forename><surname>Jeon</surname></persName><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation></author><author><persName><forename type="first">Shinrye</forename><surname>Lee</surname></persName><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation></author><author><persName><forename type="first">Ho Won</forename><surname>Lee</surname></persName><affiliation>Department of Neurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Korea</affiliation></author><author><persName><forename type="first">Je‐Yoel</forename><surname>Cho</surname></persName><affiliation>Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Korea</affiliation></author><author><persName><forename type="first">Kyoungho</forename><surname>Suk</surname></persName><note type="correspondence"><p>Correspondence: Department of Pharmacology, Kyungpook National University School of Medicine, 101 Dong‐In, Joong‐gu, Daegu, 700‐422, Korea</p></note><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation></author></analytic><monogr><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="pISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><idno type="DOI">10.1002/(ISSN)1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-08-15"></date><biblScope unit="volume">87</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="2578">2578</biblScope><biblScope unit="page" to="2590">2590</biblScope></imprint></monogr><idno type="istex">6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49</idno><idno type="DOI">10.1002/jnr.22081</idno><idno type="ArticleID">JNR22081</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Proteomic analysis of cerebrospinal fluid (CSF) samples derived from patients with Alzheimer's disease (AD) or Parkinson's disease (PD) was performed. On the basis of liquid chromatography–tandem mass spectrometry, two‐dimensional gel electrophoresis analysis, and Western blot validation, it was found that the level of soluble form of monocyte differentiation antigen CD14 precursor was elevated in CSF from AD or PD patients compared with normal subjects. The soluble CD14 protein and mRNA expression was detected in microglia cells, indicating that microglia may be a cellular source of soluble CD14 in CSF. Next, the role of soluble CD14 in the regulation of glial functions was investigated. Soluble CD14 inhibited lipopolysaccharide (LPS)‐ or LPS/interferon‐gamma‐induced nitric oxide production and cell death of microglia and astrocytes. Soluble CD14 suppressed glial neurotoxicity in a coculture of glia/neuroblastoma. In addition, soluble CD14 moderately enhanced phagocytic activity of microglia. These results suggest that microglia‐derived soluble CD14 is a candidate CSF biomarker for AD and PD, and the soluble CD14 may inhibit glial activation by interfering with LPS effects. © 2009 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>neurodegenerative diseases</term></item><item><term>cerebrospinal fluid (CSF)</term></item><item><term>liquid chromatography–tandem mass spectrometry (LC‐MS/MS)</term></item><item><term>monocyte differentiation antigen CD14 precursor</term></item><item><term>two‐dimensional gel electrophoresis (2‐DE)</term></item><item><term>glia</term></item><item><term>phagocytosis</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-02-06">Received</change><change when="2009-02-17">Registration</change><change when="2009-08-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4547</doi><issn type="print">0360-4012</issn><issn type="electronic">1097-4547</issn><idGroup><id type="product" value="JNR"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF NEUROSCIENCE RESEARCH">Journal of Neuroscience Research</title><title type="short">J. 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href="file:JNR.JNR22081.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="73"></count><count type="wordTotal" number="8835"></count></countGroup><titleGroup><title type="main" xml:lang="en">Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions</title><title type="short" xml:lang="en">Soluble CD14 Regulates Glia Functions</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Guo Nan</givenNames><familyName>Yin</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hyejin</givenNames><familyName>Jeon</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Shinrye</givenNames><familyName>Lee</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Ho Won</givenNames><familyName>Lee</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Je‐Yoel</givenNames><familyName>Cho</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Kyoungho</givenNames><familyName>Suk</familyName></personName><contactDetails><email>ksuk@knu.ac.kr</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="KR" type="organization"><unparsedAffiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="KR" type="organization"><unparsedAffiliation>Department of Neurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Korea</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="KR" type="organization"><unparsedAffiliation>Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">neurodegenerative diseases</keyword><keyword xml:id="kwd2">cerebrospinal fluid (CSF)</keyword><keyword xml:id="kwd3">liquid chromatography–tandem mass spectrometry (LC‐MS/MS)</keyword><keyword xml:id="kwd4">monocyte differentiation antigen CD14 precursor</keyword><keyword xml:id="kwd5">two‐dimensional gel electrophoresis (2‐DE)</keyword><keyword xml:id="kwd6">glia</keyword><keyword xml:id="kwd7">phagocytosis</keyword></keywordGroup><fundingInfo><fundingAgency>Basic Research Program of the Korea Science and Engineering Foundation</fundingAgency><fundingNumber>R01‐2006‐000‐10314‐0</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Bio R&D program through the Korea Science and Engineering Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Ministry of Education, Science and Technology</fundingAgency><fundingNumber>2008‐04090</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Korea Research Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Korean Government (MOEHRD, Basic Research Promotion Fund)</fundingAgency><fundingNumber>KRF‐2006‐005‐J04202</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Brain Korea 21 Project</fundingAgency></fundingInfo><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03604012:media:jnr22081:JNR_22081_sm_SuppFig1"></mediaResource><caption>Supporting Information Figure 1. Expression of CD14 protein in U87MG human glioma cells. U87MG human glioma cells were stimulated with LPS (100 ng/ml) plus IFN‐γ (50 units/ml) for 24 h, and soluble CD14 and intracellular (or membrane‐bound) CD14 proteins were detected by Western blot analysis in the conditioned media and cell lysates, respectively. Ponceau S staining was shown to confirm the equal loading of samples. A result of densitometric analysis is shown below.</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03604012:media:jnr22081:JNR_22081_sm_SuppVideo"></mediaResource><caption>Supporting Information Video 1: A three‐dimensional image showing the engulfment of zymosan A particles by microglia cells.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Proteomic analysis of cerebrospinal fluid (CSF) samples derived from patients with Alzheimer's disease (AD) or Parkinson's disease (PD) was performed. On the basis of liquid chromatography–tandem mass spectrometry, two‐dimensional gel electrophoresis analysis, and Western blot validation, it was found that the level of soluble form of monocyte differentiation antigen CD14 precursor was elevated in CSF from AD or PD patients compared with normal subjects. The soluble CD14 protein and mRNA expression was detected in microglia cells, indicating that microglia may be a cellular source of soluble CD14 in CSF. Next, the role of soluble CD14 in the regulation of glial functions was investigated. Soluble CD14 inhibited lipopolysaccharide (LPS)‐ or LPS/interferon‐gamma‐induced nitric oxide production and cell death of microglia and astrocytes. Soluble CD14 suppressed glial neurotoxicity in a coculture of glia/neuroblastoma. In addition, soluble CD14 moderately enhanced phagocytic activity of microglia. These results suggest that microglia‐derived soluble CD14 is a candidate CSF biomarker for AD and PD, and the soluble CD14 may inhibit glial activation by interfering with LPS effects. © 2009 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Soluble CD14 Regulates Glia Functions</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Role of soluble CD14 in cerebrospinal fluid as a regulator of glial functions</title></titleInfo><name type="personal"><namePart type="given">Guo Nan</namePart><namePart type="family">Yin</namePart><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hyejin</namePart><namePart type="family">Jeon</namePart><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shinrye</namePart><namePart type="family">Lee</namePart><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ho Won</namePart><namePart type="family">Lee</namePart><affiliation>Department of Neurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Je‐Yoel</namePart><namePart type="family">Cho</namePart><affiliation>Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kyoungho</namePart><namePart type="family">Suk</namePart><affiliation>Department of Pharmacology, Brain Science and Engineering Institute, CMRI, Kyungpook National University School of Medicine, Daegu, Korea</affiliation><description>Correspondence: Department of Pharmacology, Kyungpook National University School of Medicine, 101 Dong‐In, Joong‐gu, Daegu, 700‐422, Korea</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-08-15</dateIssued><dateCaptured encoding="w3cdtf">2009-02-06</dateCaptured><dateValid encoding="w3cdtf">2009-02-17</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">6</extent><extent unit="tables">2</extent><extent unit="references">73</extent><extent unit="words">8835</extent></physicalDescription><abstract lang="en">Proteomic analysis of cerebrospinal fluid (CSF) samples derived from patients with Alzheimer's disease (AD) or Parkinson's disease (PD) was performed. On the basis of liquid chromatography–tandem mass spectrometry, two‐dimensional gel electrophoresis analysis, and Western blot validation, it was found that the level of soluble form of monocyte differentiation antigen CD14 precursor was elevated in CSF from AD or PD patients compared with normal subjects. The soluble CD14 protein and mRNA expression was detected in microglia cells, indicating that microglia may be a cellular source of soluble CD14 in CSF. Next, the role of soluble CD14 in the regulation of glial functions was investigated. Soluble CD14 inhibited lipopolysaccharide (LPS)‐ or LPS/interferon‐gamma‐induced nitric oxide production and cell death of microglia and astrocytes. Soluble CD14 suppressed glial neurotoxicity in a coculture of glia/neuroblastoma. In addition, soluble CD14 moderately enhanced phagocytic activity of microglia. These results suggest that microglia‐derived soluble CD14 is a candidate CSF biomarker for AD and PD, and the soluble CD14 may inhibit glial activation by interfering with LPS effects. © 2009 Wiley‐Liss, Inc.</abstract><note type="funding">Basic Research Program of the Korea Science and Engineering Foundation - No. R01‐2006‐000‐10314‐0; </note><note type="funding">Bio R&D program through the Korea Science and Engineering Foundation</note><note type="funding">Ministry of Education, Science and Technology - No. 2008‐04090; </note><note type="funding">Korea Research Foundation</note><note type="funding">Korean Government (MOEHRD, Basic Research Promotion Fund) - No. KRF‐2006‐005‐J04202; </note><note type="funding">Brain Korea 21 Project</note><subject lang="en"><genre>Keywords</genre><topic>neurodegenerative diseases</topic><topic>cerebrospinal fluid (CSF)</topic><topic>liquid chromatography–tandem mass spectrometry (LC‐MS/MS)</topic><topic>monocyte differentiation antigen CD14 precursor</topic><topic>two‐dimensional gel electrophoresis (2‐DE)</topic><topic>glia</topic><topic>phagocytosis</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroscience Research</title></titleInfo><titleInfo type="abbreviated"><title>J. Neurosci. Res.</title></titleInfo><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information Figure 1. Expression of CD14 protein in U87MG human glioma cells. U87MG human glioma cells were stimulated with LPS (100 ng/ml) plus IFN‐γ (50 units/ml) for 24 h, and soluble CD14 and intracellular (or membrane‐bound) CD14 proteins were detected by Western blot analysis in the conditioned media and cell lysates, respectively. Ponceau S staining was shown to confirm the equal loading of samples. A result of densitometric analysis is shown below. - Supporting Information Video 1: A three‐dimensional image showing the engulfment of zymosan A particles by microglia cells. - </note><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0360-4012</identifier><identifier type="eISSN">1097-4547</identifier><identifier type="DOI">10.1002/(ISSN)1097-4547</identifier><identifier type="PublisherID">JNR</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>2578</start><end>2590</end><total>13</total></extent></part></relatedItem><identifier type="istex">6AD32FBA1BF4DAA4A4763D8F89A2A3916B679E49</identifier><identifier type="DOI">10.1002/jnr.22081</identifier><identifier type="ArticleID">JNR22081</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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