CD200R/CD200 inhibits osteoclastogenesis: new mechanism of osteoclast control by mesenchymal stem cells in human
Bone homeostasis is maintained by the balance between bone-forming osteoblasts and bone-degrading osteoclasts. Osteoblasts have a mesenchymal origin whereas osteoclasts belong to the myeloid lineage. Osteoclast and osteoblast communication occurs through soluble factors secretion, cell-bone interact...
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| description | Bone homeostasis is maintained by the balance between bone-forming osteoblasts and bone-degrading osteoclasts. Osteoblasts have a mesenchymal origin whereas osteoclasts belong to the myeloid lineage. Osteoclast and osteoblast communication occurs through soluble factors secretion, cell-bone interaction and cell-cell contact, which modulate their activities. CD200 is an immunoglobulin superfamilly member expressed on various types of cells including mesenchymal stem cells (MSCs). CD200 receptor (CD200R) is expressed on myeloid cells such as monocytes/macrophages. We assume that CD200 could be a new molecule involved in the control of osteoclastogenesis and could play a role in MSC-osteoclast communication in humans. In this study, we demonstrated that soluble CD200 inhibited the differentiation of osteoclast precursors as well as their maturation in bone-resorbing cells in vitro. Soluble CD200 did not modify the monocyte phenotype but inhibited the receptor activator of nuclear factor kappa-B ligand (RANKL) signaling pathway as well as the gene expression of osteoclast markers such as osteoclast-associated receptor (OSCAR) and nuclear factor of activated T cells cytoplasmic 1 (NFATc1). Moreover, MSCs inhibited osteoclast formation, which depended on cell-cell contact and was associated with CD200 expression on the MSC surface. Our results clearly demonstrate that MSCs, through the expression of CD200, play a major role in the regulation of bone resorption and bone physiology and that the CD200-CD200R couple could be a new target to control bone diseases. |
| doi_str_mv | 10.1371/journal.pone.0072831 |
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Osteoblasts have a mesenchymal origin whereas osteoclasts belong to the myeloid lineage. Osteoclast and osteoblast communication occurs through soluble factors secretion, cell-bone interaction and cell-cell contact, which modulate their activities. CD200 is an immunoglobulin superfamilly member expressed on various types of cells including mesenchymal stem cells (MSCs). CD200 receptor (CD200R) is expressed on myeloid cells such as monocytes/macrophages. We assume that CD200 could be a new molecule involved in the control of osteoclastogenesis and could play a role in MSC-osteoclast communication in humans. In this study, we demonstrated that soluble CD200 inhibited the differentiation of osteoclast precursors as well as their maturation in bone-resorbing cells in vitro. Soluble CD200 did not modify the monocyte phenotype but inhibited the receptor activator of nuclear factor kappa-B ligand (RANKL) signaling pathway as well as the gene expression of osteoclast markers such as osteoclast-associated receptor (OSCAR) and nuclear factor of activated T cells cytoplasmic 1 (NFATc1). Moreover, MSCs inhibited osteoclast formation, which depended on cell-cell contact and was associated with CD200 expression on the MSC surface. Our results clearly demonstrate that MSCs, through the expression of CD200, play a major role in the regulation of bone resorption and bone physiology and that the CD200-CD200R couple could be a new target to control bone diseases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0072831</identifier><identifier>PMID: 23940819</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antigens, CD - pharmacology ; Antigens, CD - physiology ; Antigens, Surface - physiology ; Arthritis ; Biocompatibility ; Biomedical materials ; Bone diseases ; Bone marrow ; Bone resorption ; Bone Resorption - genetics ; Bone surgery ; Bone turnover ; CD200 antigen ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cell interactions ; Cells, Cultured ; Cytokines ; Down-Regulation - genetics ; Gene expression ; Homeostasis ; Humans ; Kinases ; Lymphocytes ; Macrophage Colony-Stimulating Factor - pharmacology ; Macrophages ; MAP Kinase Signaling System - drug effects ; Mesenchymal stem cells ; Mesenchymal Stromal Cells - drug effects ; Mesenchymal Stromal Cells - physiology ; Mesenchyme ; Monocytes ; Monocytes - drug effects ; Monocytes - physiology ; Myeloid cells ; NF-AT protein ; Osteoblasts ; Osteoclastogenesis ; Osteoclasts ; Osteoclasts - drug effects ; Osteoclasts - physiology ; Osteoprogenitor cells ; Phosphatase ; RANK Ligand - pharmacology ; Receptors, Cell Surface - physiology ; Recombinant Proteins - pharmacology ; Regulation ; Signal transduction ; Signaling ; Stem cells ; T cells ; TRANCE protein ; Transcription factors ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2013-08, Vol.8 (8), p.e72831-e72831</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Varin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Varin et al 2013 Varin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-f8ade1bc6011687aa75d9870f78491828f0f701f3e05e1573ac2f800bf5db1083</citedby><cites>FETCH-LOGICAL-c758t-f8ade1bc6011687aa75d9870f78491828f0f701f3e05e1573ac2f800bf5db1083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733817/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733817/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23940819$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Varin, Audrey</creatorcontrib><creatorcontrib>Pontikoglou, Charalampos</creatorcontrib><creatorcontrib>Labat, Elodie</creatorcontrib><creatorcontrib>Deschaseaux, Frédéric</creatorcontrib><creatorcontrib>Sensebé, Luc</creatorcontrib><title>CD200R/CD200 inhibits osteoclastogenesis: new mechanism of osteoclast control by mesenchymal stem cells in human</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Bone homeostasis is maintained by the balance between bone-forming osteoblasts and bone-degrading osteoclasts. 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Soluble CD200 did not modify the monocyte phenotype but inhibited the receptor activator of nuclear factor kappa-B ligand (RANKL) signaling pathway as well as the gene expression of osteoclast markers such as osteoclast-associated receptor (OSCAR) and nuclear factor of activated T cells cytoplasmic 1 (NFATc1). Moreover, MSCs inhibited osteoclast formation, which depended on cell-cell contact and was associated with CD200 expression on the MSC surface. 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Soluble CD200 did not modify the monocyte phenotype but inhibited the receptor activator of nuclear factor kappa-B ligand (RANKL) signaling pathway as well as the gene expression of osteoclast markers such as osteoclast-associated receptor (OSCAR) and nuclear factor of activated T cells cytoplasmic 1 (NFATc1). Moreover, MSCs inhibited osteoclast formation, which depended on cell-cell contact and was associated with CD200 expression on the MSC surface. Our results clearly demonstrate that MSCs, through the expression of CD200, play a major role in the regulation of bone resorption and bone physiology and that the CD200-CD200R couple could be a new target to control bone diseases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23940819</pmid><doi>10.1371/journal.pone.0072831</doi><tpages>e72831</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antigens, CD - pharmacology Antigens, CD - physiology Antigens, Surface - physiology Arthritis Biocompatibility Biomedical materials Bone diseases Bone marrow Bone resorption Bone Resorption - genetics Bone surgery Bone turnover CD200 antigen Cell Differentiation - drug effects Cell Differentiation - genetics Cell interactions Cells, Cultured Cytokines Down-Regulation - genetics Gene expression Homeostasis Humans Kinases Lymphocytes Macrophage Colony-Stimulating Factor - pharmacology Macrophages MAP Kinase Signaling System - drug effects Mesenchymal stem cells Mesenchymal Stromal Cells - drug effects Mesenchymal Stromal Cells - physiology Mesenchyme Monocytes Monocytes - drug effects Monocytes - physiology Myeloid cells NF-AT protein Osteoblasts Osteoclastogenesis Osteoclasts Osteoclasts - drug effects Osteoclasts - physiology Osteoprogenitor cells Phosphatase RANK Ligand - pharmacology Receptors, Cell Surface - physiology Recombinant Proteins - pharmacology Regulation Signal transduction Signaling Stem cells T cells TRANCE protein Transcription factors Tumor necrosis factor-TNF |
| title | CD200R/CD200 inhibits osteoclastogenesis: new mechanism of osteoclast control by mesenchymal stem cells in human |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T18%3A00%3A59IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CD200R/CD200%20inhibits%20osteoclastogenesis:%20new%20mechanism%20of%20osteoclast%20control%20by%20mesenchymal%20stem%20cells%20in%20human&rft.jtitle=PloS%20one&rft.au=Varin,%20Audrey&rft.date=2013-08-05&rft.volume=8&rft.issue=8&rft.spage=e72831&rft.epage=e72831&rft.pages=e72831-e72831&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0072831&rft_dat=%3Cgale_plos_%3EA478419378%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1430247414&rft_id=info:pmid/23940819&rft_galeid=A478419378&rft_doaj_id=oai_doaj_org_article_74f510affdda4a4480ed065d8a1df824&rfr_iscdi=true |