CCL2 and CCR2 are Essential for the Formation of Osteoclasts and Foreign Body Giant Cells.
Identifieur interne : 000161 ( Main/Exploration ); précédent : 000160; suivant : 000162CCL2 and CCR2 are Essential for the Formation of Osteoclasts and Foreign Body Giant Cells.
Auteurs : Usman A. Khan [Australie] ; Saeed M. Hashimi [Australie] ; Mahmoud M. Bakr [Australie] ; Mark R. Forwood [Australie] ; Nigel A. Morrison [Australie]Source :
- Journal of cellular biochemistry [ 1097-4644 ] ; 2016.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Animaux (MeSH), Cellules cultivées (MeSH), Cellules géantes à corps étrangers (physiologie), Chimiokine CCL2 (physiologie), Expression des gènes (MeSH), Ostéoclastes (physiologie), Récepteurs CCR2 (physiologie), Récepteurs CCR3 (génétique), Récepteurs CCR3 (métabolisme), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Tibia (cytologie).
- MESH :
- cytologie : Tibia.
- génétique : ARN messager, Récepteurs CCR3.
- métabolisme : ARN messager, Récepteurs CCR3.
- physiologie : Cellules géantes à corps étrangers, Chimiokine CCL2, Ostéoclastes, Récepteurs CCR2.
- Animaux, Cellules cultivées, Expression des gènes, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), Cells, Cultured (MeSH), Chemokine CCL2 (physiology), Gene Expression (MeSH), Giant Cells, Foreign-Body (physiology), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Osteoclasts (physiology), RNA, Messenger (genetics), RNA, Messenger (metabolism), Receptors, CCR2 (physiology), Receptors, CCR3 (genetics), Receptors, CCR3 (metabolism), Tibia (cytology).
- MESH :
- chemical , genetics : RNA, Messenger, Receptors, CCR3.
- chemical , metabolism : RNA, Messenger, Receptors, CCR3.
- chemical , physiology : Chemokine CCL2, Receptors, CCR2.
- cytology : Tibia.
- physiology : Giant Cells, Foreign-Body, Osteoclasts.
- Animals, Cells, Cultured, Gene Expression, Mice, Inbred C57BL, Mice, Knockout.
Abstract
Osteoclasts are multinucleated cells responsible for bone resorption. They are derived from the fusion of cells in the monocyte/macrophage lineage. Monocytes and macrophages can also fuse to form foreign body giant cells (FBGC). Foreign body giant cells are observed at the interface between a host and a foreign body such as implants during a foreign body reaction. Macrophages are attracted to the site of bone resorption and foreign body reactions by different cytokines. Chemokine (C-C) ligand-2 (CCL2) is an important chemotactic factor and binds to a receptor CCR2. In this study we investigated the importance of CCL2 and the receptor CCR2 in the formation of osteoclasts and FBGC. CCL2 mRNA was more highly expressed in giant cell culture than macrophages, being 9-fold and 16-fold more abundant in osteoclasts and FBGC respectively. Significantly fewer osteoclasts and FBGC were cultured from the bone marrow of CCL2 and CCR2 knockout mice, when compared to wild type. Not only were the number of giant cells reduced but there was a significant reduction in the number of nuclei and the size of these cells in the cultures of CCL2 and CCR2 knockout mice. Formation of osteoclasts and FBGC were recovered in cultures by addition of exogenous CCL2 to the media containing marrow cells from CCL2-/- mice. We conclude that CCL2 and its receptor CCR2 are important for the formation of osteoclasts and FBGC and absence of these genes causes inhibition of osteoclast and FBGC formation.
DOI: 10.1002/jcb.25282
PubMed: 26205994
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">CCL2 and CCR2 are Essential for the Formation of Osteoclasts and Foreign Body Giant Cells.</title><author><name sortKey="Khan, Usman A" sort="Khan, Usman A" uniqKey="Khan U" first="Usman A" last="Khan">Usman A. Khan</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Senior Dentist Dalby Dental Clinic, Western Down, Queensland, 4405, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Senior Dentist Dalby Dental Clinic, Western Down, Queensland, 4405</wicri:regionArea><wicri:noRegion>4405</wicri:noRegion></affiliation></author><author><name sortKey="Hashimi, Saeed M" sort="Hashimi, Saeed M" uniqKey="Hashimi S" first="Saeed M" last="Hashimi">Saeed M. Hashimi</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author><author><name sortKey="Bakr, Mahmoud M" sort="Bakr, Mahmoud M" uniqKey="Bakr M" first="Mahmoud M" last="Bakr">Mahmoud M. Bakr</name><affiliation wicri:level="1"><nlm:affiliation>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author><author><name sortKey="Forwood, Mark R" sort="Forwood, Mark R" uniqKey="Forwood M" first="Mark R" last="Forwood">Mark R. Forwood</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author><author><name sortKey="Morrison, Nigel A" sort="Morrison, Nigel A" uniqKey="Morrison N" first="Nigel A" last="Morrison">Nigel A. Morrison</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26205994</idno><idno type="pmid">26205994</idno><idno type="doi">10.1002/jcb.25282</idno><idno type="wicri:Area/Main/Corpus">000172</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000172</idno><idno type="wicri:Area/Main/Curation">000172</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000172</idno><idno type="wicri:Area/Main/Exploration">000172</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">CCL2 and CCR2 are Essential for the Formation of Osteoclasts and Foreign Body Giant Cells.</title><author><name sortKey="Khan, Usman A" sort="Khan, Usman A" uniqKey="Khan U" first="Usman A" last="Khan">Usman A. Khan</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Senior Dentist Dalby Dental Clinic, Western Down, Queensland, 4405, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Senior Dentist Dalby Dental Clinic, Western Down, Queensland, 4405</wicri:regionArea><wicri:noRegion>4405</wicri:noRegion></affiliation></author><author><name sortKey="Hashimi, Saeed M" sort="Hashimi, Saeed M" uniqKey="Hashimi S" first="Saeed M" last="Hashimi">Saeed M. Hashimi</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author><author><name sortKey="Bakr, Mahmoud M" sort="Bakr, Mahmoud M" uniqKey="Bakr M" first="Mahmoud M" last="Bakr">Mahmoud M. Bakr</name><affiliation wicri:level="1"><nlm:affiliation>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author><author><name sortKey="Forwood, Mark R" sort="Forwood, Mark R" uniqKey="Forwood M" first="Mark R" last="Forwood">Mark R. Forwood</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author><author><name sortKey="Morrison, Nigel A" sort="Morrison, Nigel A" uniqKey="Morrison N" first="Nigel A" last="Morrison">Nigel A. Morrison</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215</wicri:regionArea><wicri:noRegion>4215</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of cellular biochemistry</title><idno type="eISSN">1097-4644</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Chemokine CCL2 (physiology)</term><term>Gene Expression (MeSH)</term><term>Giant Cells, Foreign-Body (physiology)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Osteoclasts (physiology)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Receptors, CCR2 (physiology)</term><term>Receptors, CCR3 (genetics)</term><term>Receptors, CCR3 (metabolism)</term><term>Tibia (cytology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Animaux (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Cellules géantes à corps étrangers (physiologie)</term><term>Chimiokine CCL2 (physiologie)</term><term>Expression des gènes (MeSH)</term><term>Ostéoclastes (physiologie)</term><term>Récepteurs CCR2 (physiologie)</term><term>Récepteurs CCR3 (génétique)</term><term>Récepteurs CCR3 (métabolisme)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term><term>Tibia (cytologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA, Messenger</term><term>Receptors, CCR3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Messenger</term><term>Receptors, CCR3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Chemokine CCL2</term><term>Receptors, CCR2</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Tibia</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Tibia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Récepteurs CCR3</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Récepteurs CCR3</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cellules géantes à corps étrangers</term><term>Chimiokine CCL2</term><term>Ostéoclastes</term><term>Récepteurs CCR2</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Giant Cells, Foreign-Body</term><term>Osteoclasts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Gene Expression</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Expression des gènes</term><term>Souris de lignée C57BL</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Osteoclasts are multinucleated cells responsible for bone resorption. They are derived from the fusion of cells in the monocyte/macrophage lineage. Monocytes and macrophages can also fuse to form foreign body giant cells (FBGC). Foreign body giant cells are observed at the interface between a host and a foreign body such as implants during a foreign body reaction. Macrophages are attracted to the site of bone resorption and foreign body reactions by different cytokines. Chemokine (C-C) ligand-2 (CCL2) is an important chemotactic factor and binds to a receptor CCR2. In this study we investigated the importance of CCL2 and the receptor CCR2 in the formation of osteoclasts and FBGC. CCL2 mRNA was more highly expressed in giant cell culture than macrophages, being 9-fold and 16-fold more abundant in osteoclasts and FBGC respectively. Significantly fewer osteoclasts and FBGC were cultured from the bone marrow of CCL2 and CCR2 knockout mice, when compared to wild type. Not only were the number of giant cells reduced but there was a significant reduction in the number of nuclei and the size of these cells in the cultures of CCL2 and CCR2 knockout mice. Formation of osteoclasts and FBGC were recovered in cultures by addition of exogenous CCL2 to the media containing marrow cells from CCL2-/- mice. We conclude that CCL2 and its receptor CCR2 are important for the formation of osteoclasts and FBGC and absence of these genes causes inhibition of osteoclast and FBGC formation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26205994</PMID><DateCompleted><Year>2016</Year><Month>10</Month><Day>31</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1097-4644</ISSN><JournalIssue CitedMedium="Internet"><Volume>117</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Journal of cellular biochemistry</Title><ISOAbbreviation>J Cell Biochem</ISOAbbreviation></Journal><ArticleTitle>CCL2 and CCR2 are Essential for the Formation of Osteoclasts and Foreign Body Giant Cells.</ArticleTitle><Pagination><MedlinePgn>382-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/jcb.25282</ELocationID><Abstract><AbstractText>Osteoclasts are multinucleated cells responsible for bone resorption. They are derived from the fusion of cells in the monocyte/macrophage lineage. Monocytes and macrophages can also fuse to form foreign body giant cells (FBGC). Foreign body giant cells are observed at the interface between a host and a foreign body such as implants during a foreign body reaction. Macrophages are attracted to the site of bone resorption and foreign body reactions by different cytokines. Chemokine (C-C) ligand-2 (CCL2) is an important chemotactic factor and binds to a receptor CCR2. In this study we investigated the importance of CCL2 and the receptor CCR2 in the formation of osteoclasts and FBGC. CCL2 mRNA was more highly expressed in giant cell culture than macrophages, being 9-fold and 16-fold more abundant in osteoclasts and FBGC respectively. Significantly fewer osteoclasts and FBGC were cultured from the bone marrow of CCL2 and CCR2 knockout mice, when compared to wild type. Not only were the number of giant cells reduced but there was a significant reduction in the number of nuclei and the size of these cells in the cultures of CCL2 and CCR2 knockout mice. Formation of osteoclasts and FBGC were recovered in cultures by addition of exogenous CCL2 to the media containing marrow cells from CCL2-/- mice. We conclude that CCL2 and its receptor CCR2 are important for the formation of osteoclasts and FBGC and absence of these genes causes inhibition of osteoclast and FBGC formation.</AbstractText><CopyrightInformation>© 2015 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>Usman A</ForeName><Initials>UA</Initials><AffiliationInfo><Affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Senior Dentist Dalby Dental Clinic, Western Down, Queensland, 4405, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hashimi</LastName><ForeName>Saeed M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bakr</LastName><ForeName>Mahmoud M</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Regenerative Medicine Centre, Molecular Basis for Disease, School of Dentistry and Oral Health, Menzies Health Institute Queensland, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Forwood</LastName><ForeName>Mark R</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morrison</LastName><ForeName>Nigel A</ForeName><Initials>NA</Initials><AffiliationInfo><Affiliation>School of Medical Science, Griffith University Gold Coast Campus, Queensland, 4215, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Cell Biochem</MedlineTA><NlmUniqueID>8205768</NlmUniqueID><ISSNLinking>0730-2312</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491768">Ccl2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C515335">Ccr2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C515351">Ccr3 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018932">Chemokine CCL2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054390">Receptors, CCR2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054397">Receptors, CCR3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018932" MajorTopicYN="N">Chemokine CCL2</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015743" MajorTopicYN="N">Giant Cells, Foreign-Body</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010010" MajorTopicYN="N">Osteoclasts</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054390" MajorTopicYN="N">Receptors, CCR2</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054397" MajorTopicYN="N">Receptors, CCR3</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013977" MajorTopicYN="N">Tibia</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CCL2</Keyword><Keyword MajorTopicYN="N">CCR2</Keyword><Keyword MajorTopicYN="N">CELL DIFFERENTIATION</Keyword><Keyword MajorTopicYN="N">CELL SIGNALLING</Keyword><Keyword MajorTopicYN="N">CHEMOKINE</Keyword><Keyword MajorTopicYN="N">MACROPHAGE</Keyword><Keyword MajorTopicYN="N">OSTEOCLASTS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>07</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>07</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>7</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>7</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26205994</ArticleId><ArticleId IdType="doi">10.1002/jcb.25282</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Khan, Usman A" sort="Khan, Usman A" uniqKey="Khan U" first="Usman A" last="Khan">Usman A. Khan</name></noRegion><name sortKey="Bakr, Mahmoud M" sort="Bakr, Mahmoud M" uniqKey="Bakr M" first="Mahmoud M" last="Bakr">Mahmoud M. Bakr</name><name sortKey="Forwood, Mark R" sort="Forwood, Mark R" uniqKey="Forwood M" first="Mark R" last="Forwood">Mark R. Forwood</name><name sortKey="Hashimi, Saeed M" sort="Hashimi, Saeed M" uniqKey="Hashimi S" first="Saeed M" last="Hashimi">Saeed M. Hashimi</name><name sortKey="Hashimi, Saeed M" sort="Hashimi, Saeed M" uniqKey="Hashimi S" first="Saeed M" last="Hashimi">Saeed M. Hashimi</name><name sortKey="Khan, Usman A" sort="Khan, Usman A" uniqKey="Khan U" first="Usman A" last="Khan">Usman A. Khan</name><name sortKey="Morrison, Nigel A" sort="Morrison, Nigel A" uniqKey="Morrison N" first="Nigel A" last="Morrison">Nigel A. Morrison</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SuicidDentistV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000161 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000161 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= SuicidDentistV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:26205994
|texte= CCL2 and CCR2 are Essential for the Formation of Osteoclasts and Foreign Body Giant Cells.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:26205994" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a SuicidDentistV1
| This area was generated with Dilib version V0.6.39. |  |