Role of colony‐stimulating factor‐1 in bone metabolism
Identifieur interne : 006389 ( Istex/Corpus ); précédent : 006388; suivant : 006390Role of colony‐stimulating factor‐1 in bone metabolism
Auteurs : Rolf Felix ; Willy Hofstetter ; Antoinette Wetterwald ; Marco G. Cecchini ; Herbert FleischSource :
- Journal of Cellular Biochemistry [ 0730-2312 ] ; 1994-07.
English descriptors
- KwdEn :
- Amino acids, Binding sites, Bone metabolism, Bone resorption, Cecchini, Cell membrane, Cell populations, Cytokine, Exon, Extracellular matrix, Fleisch, Growth factor, Growth factors, Hemopoietic, Hofstetter, Long bones, Macrophage, Macrophage factor, Macrophage populations, Matrix, Mature osteoclasts, Metatarsal, Molecular forms, Mononuclear, Mrna, Murine, Opiop, Oplop, Oplop animals, Oplop mice, Oplop mouse, Osteoblast, Osteoclast, Osteoclast development, Osteoclast formation, Osteoclastic, Osteoclastic precursors, Osteoclastogenesis, Osteopetrosis, Osteopetrotic, Osteopetrotic phenotype, Precursor, Receptor, Resorbing cells, Resorption, Single injection, Strain oplop, Takahashi, Target cells, Tissue macrophages, Tlltl rats, Transcript, Translation product.
- Teeft :
- Amino acids, Binding sites, Bone metabolism, Bone resorption, Cecchini, Cell membrane, Cell populations, Cytokine, Exon, Extracellular matrix, Fleisch, Growth factor, Growth factors, Hemopoietic, Hofstetter, Long bones, Macrophage, Macrophage factor, Macrophage populations, Matrix, Mature osteoclasts, Metatarsal, Molecular forms, Mononuclear, Mrna, Murine, Opiop, Oplop, Oplop animals, Oplop mice, Oplop mouse, Osteoblast, Osteoclast, Osteoclast development, Osteoclast formation, Osteoclastic, Osteoclastic precursors, Osteoclastogenesis, Osteopetrosis, Osteopetrotic, Osteopetrotic phenotype, Precursor, Receptor, Resorbing cells, Resorption, Single injection, Strain oplop, Takahashi, Target cells, Tissue macrophages, Tlltl rats, Transcript, Translation product.
Abstract
Colony‐stimulating factor‐1 (CSF‐1) is a cytokine required for proliferation, differentiation, activity, and survival of cells of the mononuclear phagocytic system. The growth factor is synthesized as a soluble, matrix, or membrane associated molecule. The specific functions of these forms are not clear. However, some data suggest a dependence of the development of various populations of tissue macrophages on the locally expressed and presented cytokine. Deficiency in CSF‐1, as is the case in the murine mutant strain op/op, results in low numbers of macrophages and monocytes and, most striking, leads to osteopetrosis due to a virtual absence of osteoclasts. Using the op/op mutation as a model, CSF‐1 was established as one of the growth factors for osteoclasts. The expression of CSF‐1 receptors, encoded by the proto‐oncogene c‐fms, by osteoclast precursors and osteoclasts, suggested an effect of this cytokine not only during osteoclast formation but also on the mature cells. In fact, CSF‐1 was shown to inhibit the resorbing activity, to stimulate migration, and to support survival of isolated osteoclasts in vitro. By these actions on cells of the osteoclast lineage, CSF‐1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. During these processes, locally expressed and presented forms of the growth factor may play a crucial role, as will be discussed in this article. © 1994 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jcb.240550311
Links to Exploration step
ISTEX:C8E890651725622D22651B590F711FB11DD0F148Le document en format XML
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By these actions on cells of the osteoclast lineage, CSF‐1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. 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Cecchini</name><affiliations><json:string>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</json:string></affiliations></json:item><json:item><name>Herbert Fleisch</name><affiliations><json:string>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>osteoclast formation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>resorption</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CSF‐1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>bone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cytokine</value></json:item></subject><articleId><json:string>JCB240550311</json:string></articleId><arkIstex>ark:/67375/WNG-84PWH30K-Q</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Colony‐stimulating factor‐1 (CSF‐1) is a cytokine required for proliferation, differentiation, activity, and survival of cells of the mononuclear phagocytic system. The growth factor is synthesized as a soluble, matrix, or membrane associated molecule. The specific functions of these forms are not clear. However, some data suggest a dependence of the development of various populations of tissue macrophages on the locally expressed and presented cytokine. Deficiency in CSF‐1, as is the case in the murine mutant strain op/op, results in low numbers of macrophages and monocytes and, most striking, leads to osteopetrosis due to a virtual absence of osteoclasts. Using the op/op mutation as a model, CSF‐1 was established as one of the growth factors for osteoclasts. The expression of CSF‐1 receptors, encoded by the proto‐oncogene c‐fms, by osteoclast precursors and osteoclasts, suggested an effect of this cytokine not only during osteoclast formation but also on the mature cells. In fact, CSF‐1 was shown to inhibit the resorbing activity, to stimulate migration, and to support survival of isolated osteoclasts in vitro. By these actions on cells of the osteoclast lineage, CSF‐1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. During these processes, locally expressed and presented forms of the growth factor may play a crucial role, as will be discussed in this article. © 1994 Wiley‐Liss, Inc.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>233</abstractWordCount><abstractCharCount>1524</abstractCharCount><keywordCount>5</keywordCount><score>9.796</score><pdfWordCount>5769</pdfWordCount><pdfCharCount>37129</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>576 x 792 pts</pdfPageSize></qualityIndicators><title>Role of colony‐stimulating factor‐1 in bone metabolism</title><pmid><json:string>7962166</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Cellular Biochemistry</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1097-4644</json:string></doi><issn><json:string>0730-2312</json:string></issn><eissn><json:string>1097-4644</json:string></eissn><publisherId><json:string>JCB</json:string></publisherId><volume>55</volume><issue>3</issue><pages><first>340</first><last>349</last><total>10</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Prospect</value></json:item></subject></host><namedEntities><unitex><date><json:string>1994</json:string><json:string>1988</json:string></date><geogName></geogName><orgName><json:string>University of Bern</json:string><json:string>Switzerland Colony</json:string><json:string>Wiley-Liss, Inc</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Antoinette Wetterwald</json:string><json:string>Marco G. Cecchini</json:string><json:string>I. Differentiation</json:string><json:string>R. Felix</json:string><json:string>Willy Hofstetter</json:string></persName><placeName><json:string>Switzerland</json:string><json:string>Bern</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Wiktor-Jedrzejczak et al., 19821</json:string><json:string>Morohashi et al., 19941</json:string><json:string>[1251]</json:string><json:string>Sundquist et al., 19931</json:string><json:string>Marks and Lane, 1976</json:string><json:string>Wink et al., 1991</json:string><json:string>Felix et al.</json:string><json:string>Felix et al., 1990</json:string><json:string>Marks et al., 19921</json:string><json:string>Takahashi et al., 1991a</json:string><json:string>Kodama et al., 19911</json:string><json:string>Wiktor-Jedrzejczak et al., 19901</json:string><json:string>Rodriguiz et al., 19931</json:string><json:string>Broxmeyer et al., 19911</json:string><json:string>[1991]</json:string><json:string>Marks et al., 19931</json:string><json:string>Felix et al., 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19901</json:string><json:string>Poshida et al., 1990</json:string><json:string>Rettenmier et al., 19871</json:string><json:string>Hofstetter et al., 19931</json:string><json:string>Stanley et al., 19831</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-84PWH30K-Q</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - cell biology</json:string><json:string>2 - biochemistry & molecular biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - biochemistry & molecular biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cell Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Molecular 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key="CH"></country></address></affiliation><affiliation>Dept. of Pathophysiology, University of Bern, Murtenstrasse 35, CH‐3010 Bern, Switzerland</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Willy</forename><surname>Hofstetter</surname></persName><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland<address><country key="CH"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Antoinette</forename><surname>Wetterwald</surname></persName><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland<address><country key="CH"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Marco G.</forename><surname>Cecchini</surname></persName><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland<address><country key="CH"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Herbert</forename><surname>Fleisch</surname></persName><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland<address><country key="CH"></country></address></affiliation></author><idno type="istex">C8E890651725622D22651B590F711FB11DD0F148</idno><idno type="ark">ark:/67375/WNG-84PWH30K-Q</idno><idno type="DOI">10.1002/jcb.240550311</idno><idno type="unit">JCB240550311</idno><idno type="toTypesetVersion">file:JCB.JCB240550311.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Cellular Biochemistry</title><title level="j" type="alt">JOURNAL OF CELLULAR BIOCHEMISTRY</title><idno type="pISSN">0730-2312</idno><idno type="eISSN">1097-4644</idno><idno type="book-DOI">10.1002/(ISSN)1097-4644</idno><idno type="book-part-DOI">10.1002/jcb.v55:3</idno><idno type="product">JCB</idno><imprint><biblScope unit="vol">55</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="340">340</biblScope><biblScope unit="page" to="349">349</biblScope><biblScope unit="page-count">10</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1994-07"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>Colony‐stimulating factor‐1 (CSF‐1) is a cytokine required for proliferation, differentiation, activity, and survival of cells of the mononuclear phagocytic system. The growth factor is synthesized as a soluble, matrix, or membrane associated molecule. The specific functions of these forms are not clear. However, some data suggest a dependence of the development of various populations of tissue macrophages on the locally expressed and presented cytokine. Deficiency in CSF‐1, as is the case in the murine mutant strain <hi rend="italic">op</hi>/<hi rend="italic">op</hi>, results in low numbers of macrophages and monocytes and, most striking, leads to osteopetrosis due to a virtual absence of osteoclasts. Using the <hi rend="italic">op</hi>/<hi rend="italic">op</hi> mutation as a model, CSF‐1 was established as one of the growth factors for osteoclasts. The expression of CSF‐1 receptors, encoded by the proto‐oncogene <hi rend="italic">c</hi>‐<hi rend="italic">fms</hi>, by osteoclast precursors and osteoclasts, suggested an effect of this cytokine not only during osteoclast formation but also on the mature cells. In fact, CSF‐1 was shown to inhibit the resorbing activity, to stimulate migration, and to support survival of isolated osteoclasts in vitro. By these actions on cells of the osteoclast lineage, CSF‐1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. During these processes, locally expressed and presented forms of the growth factor may play a crucial role, as will be discussed in this article. © 1994 Wiley‐Liss, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">osteoclast formation</term><term xml:id="kwd2">resorption</term><term xml:id="kwd3">CSF‐1</term><term xml:id="kwd4">bone</term><term xml:id="kwd5">cytokine</term></keywords><keywords rend="articleCategory"><term>Prospect</term></keywords><keywords rend="tocHeading1"><term>Prospects</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C8E890651725622D22651B590F711FB11DD0F148/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)1097-4644</doi><issn type="print">0730-2312</issn><issn type="electronic">1097-4644</issn><idGroup><id type="product" value="JCB"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF CELLULAR BIOCHEMISTRY">Journal of Cellular Biochemistry</title><title type="short">J. Cell. Biochem.</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/jcb.v55:3</doi><numberingGroup><numbering type="journalVolume" number="55">55</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="1994-07">July 1994</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="11" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jcb.240550311</doi><idGroup><id type="unit" value="JCB240550311"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Prospect</title><title type="tocHeading1">Prospects</title></titleGroup><copyright ownership="publisher">Copyright © 1994 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="1994-01-10"></event><event type="manuscriptAccepted" date="1994-01-18"></event><event type="firstOnline" date="2004-02-19"></event><event type="publishedOnlineFinalForm" date="2004-02-19"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-29"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-23"></event></eventGroup><numberingGroup><numbering type="pageFirst">340</numbering><numbering type="pageLast">349</numbering></numberingGroup><correspondenceTo>Dept. of Pathophysiology, University of Bern, Murtenstrasse 35, CH‐3010 Bern, Switzerland</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCB.JCB240550311.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="45"></count></countGroup><titleGroup><title type="main" xml:lang="en">Role of colony‐stimulating factor‐1 in bone metabolism</title><title type="short" xml:lang="en">CSF‐1 in Bone Metabolism</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Rolf</givenNames><familyName>Felix</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Willy</givenNames><familyName>Hofstetter</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Antoinette</givenNames><familyName>Wetterwald</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marco G.</givenNames><familyName>Cecchini</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Herbert</givenNames><familyName>Fleisch</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CH" type="organization"><unparsedAffiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">osteoclast formation</keyword><keyword xml:id="kwd2">resorption</keyword><keyword xml:id="kwd3">CSF‐1</keyword><keyword xml:id="kwd4">bone</keyword><keyword xml:id="kwd5">cytokine</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Colony‐stimulating factor‐1 (CSF‐1) is a cytokine required for proliferation, differentiation, activity, and survival of cells of the mononuclear phagocytic system. The growth factor is synthesized as a soluble, matrix, or membrane associated molecule. The specific functions of these forms are not clear. However, some data suggest a dependence of the development of various populations of tissue macrophages on the locally expressed and presented cytokine. Deficiency in CSF‐1, as is the case in the murine mutant strain <i>op</i>/<i>op</i>, results in low numbers of macrophages and monocytes and, most striking, leads to osteopetrosis due to a virtual absence of osteoclasts. Using the <i>op</i>/<i>op</i> mutation as a model, CSF‐1 was established as one of the growth factors for osteoclasts. The expression of CSF‐1 receptors, encoded by the proto‐oncogene <i>c</i>‐<i>fms</i>, by osteoclast precursors and osteoclasts, suggested an effect of this cytokine not only during osteoclast formation but also on the mature cells. In fact, CSF‐1 was shown to inhibit the resorbing activity, to stimulate migration, and to support survival of isolated osteoclasts in vitro. By these actions on cells of the osteoclast lineage, CSF‐1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. During these processes, locally expressed and presented forms of the growth factor may play a crucial role, as will be discussed in this article. © 1994 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of colony‐stimulating factor‐1 in bone metabolism</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CSF‐1 in Bone Metabolism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Role of colony‐stimulating factor‐1 in bone metabolism</title></titleInfo><name type="personal"><namePart type="given">Rolf</namePart><namePart type="family">Felix</namePart><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</affiliation><affiliation>Correspondence address: Dept. of Pathophysiology, University of Bern, Murtenstrasse 35, CH‐3010 Bern, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Willy</namePart><namePart type="family">Hofstetter</namePart><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Antoinette</namePart><namePart type="family">Wetterwald</namePart><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marco G.</namePart><namePart type="family">Cecchini</namePart><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Herbert</namePart><namePart type="family">Fleisch</namePart><affiliation>Department of Pathophysiology, University of Bern, CH‐3010 Bern, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1994-07</dateIssued><dateCaptured encoding="w3cdtf">1994-01-10</dateCaptured><dateValid encoding="w3cdtf">1994-01-18</dateValid><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">3</extent><extent unit="tables">1</extent><extent unit="references">45</extent></physicalDescription><abstract lang="en">Colony‐stimulating factor‐1 (CSF‐1) is a cytokine required for proliferation, differentiation, activity, and survival of cells of the mononuclear phagocytic system. The growth factor is synthesized as a soluble, matrix, or membrane associated molecule. The specific functions of these forms are not clear. However, some data suggest a dependence of the development of various populations of tissue macrophages on the locally expressed and presented cytokine. Deficiency in CSF‐1, as is the case in the murine mutant strain op/op, results in low numbers of macrophages and monocytes and, most striking, leads to osteopetrosis due to a virtual absence of osteoclasts. Using the op/op mutation as a model, CSF‐1 was established as one of the growth factors for osteoclasts. The expression of CSF‐1 receptors, encoded by the proto‐oncogene c‐fms, by osteoclast precursors and osteoclasts, suggested an effect of this cytokine not only during osteoclast formation but also on the mature cells. In fact, CSF‐1 was shown to inhibit the resorbing activity, to stimulate migration, and to support survival of isolated osteoclasts in vitro. By these actions on cells of the osteoclast lineage, CSF‐1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. During these processes, locally expressed and presented forms of the growth factor may play a crucial role, as will be discussed in this article. © 1994 Wiley‐Liss, Inc.</abstract><subject lang="en"><genre>keywords</genre><topic>osteoclast formation</topic><topic>resorption</topic><topic>CSF‐1</topic><topic>bone</topic><topic>cytokine</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Cellular Biochemistry</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. 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