SDF-1 promotes endochondral bone repair during fracture healing at the traumatic brain injury condition
The objective of this study was to investigate the role of stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4, on bone healing and whether SDF-1 contributes to accelerating bone repair in traumatic brain injury (TBI)/fracture model. Real-time polymerase chain reaction and immunohistochemi...
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| creator | Liu, Xiaoqi Zhou, Changlong Li, Yanjing Ji, Ye Xu, Gongping Wang, Xintao Yan, Jinglong |
| description | The objective of this study was to investigate the role of stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4, on bone healing and whether SDF-1 contributes to accelerating bone repair in traumatic brain injury (TBI)/fracture model.
Real-time polymerase chain reaction and immunohistochemical analysis were used to detect the expression of SDF-1 during the repair of femoral bone in TBI/fracture model. The TBI/fracture model was treated with anti-SDF-1 neutralizing antibody or AMD3100, an antagonist for CXCR4, and evaluated by histomorphometry. In vitro and in vivo migration assays were used to evaluate the functional effect of SDF-1 on primary mesenchymal stem cells.
The expression of SDF1 and CXCR4 messenger RNA was increased during the bone healing in TBI/fracture model but was less increased in fracture only model. High expression of SDF-1 protein was observed in the surrounding tissue of the damaged bone. Treated with anti-SDF-1 antibody or AMD3100 could inhibit new bone formation. SDF-1 increased mesenchymal stem cell chemotaxis in vitro in a dose-dependent manner. The in vivo migration study demonstrated that mesenchymal stem cells recruited by SDF-1 participate in endochondral bone repair.
The SDF-1/CXCR4 axis plays a crucial role in the accelerating fracture healing under the condition of TBI and contributes to endochondral bone repair. |
| doi_str_mv | 10.1371/journal.pone.0054077 |
| format | Article |
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Real-time polymerase chain reaction and immunohistochemical analysis were used to detect the expression of SDF-1 during the repair of femoral bone in TBI/fracture model. The TBI/fracture model was treated with anti-SDF-1 neutralizing antibody or AMD3100, an antagonist for CXCR4, and evaluated by histomorphometry. In vitro and in vivo migration assays were used to evaluate the functional effect of SDF-1 on primary mesenchymal stem cells.
The expression of SDF1 and CXCR4 messenger RNA was increased during the bone healing in TBI/fracture model but was less increased in fracture only model. High expression of SDF-1 protein was observed in the surrounding tissue of the damaged bone. Treated with anti-SDF-1 antibody or AMD3100 could inhibit new bone formation. SDF-1 increased mesenchymal stem cell chemotaxis in vitro in a dose-dependent manner. The in vivo migration study demonstrated that mesenchymal stem cells recruited by SDF-1 participate in endochondral bone repair.
The SDF-1/CXCR4 axis plays a crucial role in the accelerating fracture healing under the condition of TBI and contributes to endochondral bone repair.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0054077</identifier><identifier>PMID: 23349789</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Antibodies ; Antibodies, Neutralizing - immunology ; Antibodies, Neutralizing - pharmacology ; Biology ; Bone growth ; Bone healing ; Bone histomorphometry ; Bone marrow ; Bone surgery ; Brain ; Brain injuries ; Brain Injuries - genetics ; Brain Injuries - metabolism ; Cell migration ; Cell Movement - drug effects ; Cells, Cultured ; Chemokine CXCL12 - genetics ; Chemokine CXCL12 - immunology ; Chemokine CXCL12 - metabolism ; Chemokines ; Chemotaxis ; Chemotaxis - drug effects ; CXCR4 protein ; Endochondral bone ; Engineering ; Femur ; Femur - drug effects ; Femur - injuries ; Femur - metabolism ; Fracture Healing - drug effects ; Fracture Healing - genetics ; Fracture repair ; Fractures (Injuries) ; Gene Expression ; Growth factors ; Head injuries ; Healing ; Heart attacks ; Heterocyclic Compounds - pharmacology ; Immunohistochemistry ; In vivo methods and tests ; Medical research ; Medicine ; Mesenchymal stem cells ; Mesenchymal Stem Cells - drug effects ; Mesenchymal Stem Cells - metabolism ; Mesenchyme ; Mice ; Mice, Inbred C57BL ; mRNA ; Orthopedics ; Osteogenesis ; Polymerase chain reaction ; Receptors, CXCR4 - antagonists & inhibitors ; Receptors, CXCR4 - genetics ; Receptors, CXCR4 - metabolism ; Recombinant Proteins - pharmacology ; Repair ; Researchers ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonucleic acid ; RNA ; Rodents ; SDF-1 protein ; Stem cells ; Studies ; Time Factors ; Traumatic brain injury</subject><ispartof>PloS one, 2013-01, Vol.8 (1), p.e54077-e54077</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Liu 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 Liu et al 2013 Liu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6587-c569f139f49ea7bbd46bc887a0a54cb9ab6eb00fe94e1dfe33aa58b08a19f1063</citedby><cites>FETCH-LOGICAL-c6587-c569f139f49ea7bbd46bc887a0a54cb9ab6eb00fe94e1dfe33aa58b08a19f1063</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/PMC3551938/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551938/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23349789$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xiaoqi</creatorcontrib><creatorcontrib>Zhou, Changlong</creatorcontrib><creatorcontrib>Li, Yanjing</creatorcontrib><creatorcontrib>Ji, Ye</creatorcontrib><creatorcontrib>Xu, Gongping</creatorcontrib><creatorcontrib>Wang, Xintao</creatorcontrib><creatorcontrib>Yan, Jinglong</creatorcontrib><title>SDF-1 promotes endochondral bone repair during fracture healing at the traumatic brain injury condition</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The objective of this study was to investigate the role of stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4, on bone healing and whether SDF-1 contributes to accelerating bone repair in traumatic brain injury (TBI)/fracture model.
Real-time polymerase chain reaction and immunohistochemical analysis were used to detect the expression of SDF-1 during the repair of femoral bone in TBI/fracture model. The TBI/fracture model was treated with anti-SDF-1 neutralizing antibody or AMD3100, an antagonist for CXCR4, and evaluated by histomorphometry. In vitro and in vivo migration assays were used to evaluate the functional effect of SDF-1 on primary mesenchymal stem cells.
The expression of SDF1 and CXCR4 messenger RNA was increased during the bone healing in TBI/fracture model but was less increased in fracture only model. High expression of SDF-1 protein was observed in the surrounding tissue of the damaged bone. Treated with anti-SDF-1 antibody or AMD3100 could inhibit new bone formation. SDF-1 increased mesenchymal stem cell chemotaxis in vitro in a dose-dependent manner. The in vivo migration study demonstrated that mesenchymal stem cells recruited by SDF-1 participate in endochondral bone repair.
The SDF-1/CXCR4 axis plays a crucial role in the accelerating fracture healing under the condition of TBI and contributes to endochondral bone repair.</description><subject>Analysis</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antibodies, Neutralizing - immunology</subject><subject>Antibodies, Neutralizing - pharmacology</subject><subject>Biology</subject><subject>Bone growth</subject><subject>Bone healing</subject><subject>Bone histomorphometry</subject><subject>Bone marrow</subject><subject>Bone surgery</subject><subject>Brain</subject><subject>Brain injuries</subject><subject>Brain Injuries - genetics</subject><subject>Brain Injuries - metabolism</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL12 - genetics</subject><subject>Chemokine CXCL12 - immunology</subject><subject>Chemokine CXCL12 - metabolism</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>Chemotaxis - drug effects</subject><subject>CXCR4 protein</subject><subject>Endochondral bone</subject><subject>Engineering</subject><subject>Femur</subject><subject>Femur - drug effects</subject><subject>Femur - injuries</subject><subject>Femur - metabolism</subject><subject>Fracture Healing - drug effects</subject><subject>Fracture Healing - genetics</subject><subject>Fracture repair</subject><subject>Fractures (Injuries)</subject><subject>Gene Expression</subject><subject>Growth factors</subject><subject>Head injuries</subject><subject>Healing</subject><subject>Heart attacks</subject><subject>Heterocyclic Compounds - pharmacology</subject><subject>Immunohistochemistry</subject><subject>In vivo methods and tests</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stem Cells - drug effects</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>mRNA</subject><subject>Orthopedics</subject><subject>Osteogenesis</subject><subject>Polymerase chain reaction</subject><subject>Receptors, CXCR4 - antagonists & inhibitors</subject><subject>Receptors, CXCR4 - genetics</subject><subject>Receptors, CXCR4 - metabolism</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Repair</subject><subject>Researchers</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>SDF-1 protein</subject><subject>Stem cells</subject><subject>Studies</subject><subject>Time Factors</subject><subject>Traumatic brain injury</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk1Fr1TAUx4sobk6_gWhAEH2416Rpk-ZFGNPphcHAqa_hNEl7c2mTu6QV9-1Nvd1YZQ_Sh5bT3_9_cs7JybKXBK8J5eTDzo_BQbfee2fWGJcF5vxRdkwEzVcsx_Txve-j7FmMuwTRirGn2VFOaSF4JY6z9urT-YqgffC9H0xExmmvtt7pAB2qkzUKZg82ID0G61rUBFDDGAzaGuimAAxo2Bo0BBh7GKxCdQDrkHW7MdwglZzsYL17nj1poIvmxfw-yX6cf_5-9nV1cfllc3Z6sVKsrPhKlUw0hIqmEAZ4XeuC1aqqOGAoC1ULqJmpMW6MKAzRjaEUoKxqXAFJOszoSfb64LvvfJRzj6IkNOdciJzxRGwOhPawk_tgewg30oOVfwM-tBJCKqQzUmmoSsZLQau8yBkRgqsixSjmRGs9Zfs4Zxvr3mhlXOpDtzBd_nF2K1v_S9KyTMOpksG72SD469HEQfY2KtN14Iwf07nzKsdFTsV07jf_oA9XN1MtpAKsa3zKqyZTeVrwijBOME3U-gEqPdr0Ns3MNDbFF4L3C0FiBvN7aGGMUW6uvv0_e_lzyb69x053athG343TlYlLsDiAKvgYg2numkywnPbhthty2gc570OSvbo_oDvR7QLQPxHcBeg</recordid><startdate>20130122</startdate><enddate>20130122</enddate><creator>Liu, Xiaoqi</creator><creator>Zhou, Changlong</creator><creator>Li, Yanjing</creator><creator>Ji, Ye</creator><creator>Xu, Gongping</creator><creator>Wang, Xintao</creator><creator>Yan, Jinglong</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130122</creationdate><title>SDF-1 promotes endochondral bone repair during fracture healing at the traumatic brain injury condition</title><author>Liu, Xiaoqi ; Zhou, Changlong ; Li, Yanjing ; Ji, Ye ; Xu, Gongping ; Wang, Xintao ; Yan, Jinglong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6587-c569f139f49ea7bbd46bc887a0a54cb9ab6eb00fe94e1dfe33aa58b08a19f1063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antibodies, Neutralizing - immunology</topic><topic>Antibodies, Neutralizing - pharmacology</topic><topic>Biology</topic><topic>Bone growth</topic><topic>Bone healing</topic><topic>Bone histomorphometry</topic><topic>Bone marrow</topic><topic>Bone surgery</topic><topic>Brain</topic><topic>Brain injuries</topic><topic>Brain Injuries - genetics</topic><topic>Brain Injuries - metabolism</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cells, Cultured</topic><topic>Chemokine CXCL12 - genetics</topic><topic>Chemokine CXCL12 - immunology</topic><topic>Chemokine CXCL12 - metabolism</topic><topic>Chemokines</topic><topic>Chemotaxis</topic><topic>Chemotaxis - drug effects</topic><topic>CXCR4 protein</topic><topic>Endochondral bone</topic><topic>Engineering</topic><topic>Femur</topic><topic>Femur - drug effects</topic><topic>Femur - injuries</topic><topic>Femur - metabolism</topic><topic>Fracture Healing - drug effects</topic><topic>Fracture Healing - genetics</topic><topic>Fracture repair</topic><topic>Fractures (Injuries)</topic><topic>Gene Expression</topic><topic>Growth factors</topic><topic>Head injuries</topic><topic>Healing</topic><topic>Heart attacks</topic><topic>Heterocyclic Compounds - pharmacology</topic><topic>Immunohistochemistry</topic><topic>In vivo methods and tests</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stem Cells - drug effects</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Mesenchyme</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>mRNA</topic><topic>Orthopedics</topic><topic>Osteogenesis</topic><topic>Polymerase chain reaction</topic><topic>Receptors, CXCR4 - antagonists & inhibitors</topic><topic>Receptors, CXCR4 - genetics</topic><topic>Receptors, CXCR4 - metabolism</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Repair</topic><topic>Researchers</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Rodents</topic><topic>SDF-1 protein</topic><topic>Stem cells</topic><topic>Studies</topic><topic>Time Factors</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Xiaoqi</creatorcontrib><creatorcontrib>Zhou, Changlong</creatorcontrib><creatorcontrib>Li, Yanjing</creatorcontrib><creatorcontrib>Ji, Ye</creatorcontrib><creatorcontrib>Xu, Gongping</creatorcontrib><creatorcontrib>Wang, Xintao</creatorcontrib><creatorcontrib>Yan, Jinglong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Xiaoqi</au><au>Zhou, Changlong</au><au>Li, Yanjing</au><au>Ji, Ye</au><au>Xu, Gongping</au><au>Wang, Xintao</au><au>Yan, Jinglong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SDF-1 promotes endochondral bone repair during fracture healing at the traumatic brain injury condition</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-01-22</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>e54077</spage><epage>e54077</epage><pages>e54077-e54077</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The objective of this study was to investigate the role of stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4, on bone healing and whether SDF-1 contributes to accelerating bone repair in traumatic brain injury (TBI)/fracture model.
Real-time polymerase chain reaction and immunohistochemical analysis were used to detect the expression of SDF-1 during the repair of femoral bone in TBI/fracture model. The TBI/fracture model was treated with anti-SDF-1 neutralizing antibody or AMD3100, an antagonist for CXCR4, and evaluated by histomorphometry. In vitro and in vivo migration assays were used to evaluate the functional effect of SDF-1 on primary mesenchymal stem cells.
The expression of SDF1 and CXCR4 messenger RNA was increased during the bone healing in TBI/fracture model but was less increased in fracture only model. High expression of SDF-1 protein was observed in the surrounding tissue of the damaged bone. Treated with anti-SDF-1 antibody or AMD3100 could inhibit new bone formation. SDF-1 increased mesenchymal stem cell chemotaxis in vitro in a dose-dependent manner. The in vivo migration study demonstrated that mesenchymal stem cells recruited by SDF-1 participate in endochondral bone repair.
The SDF-1/CXCR4 axis plays a crucial role in the accelerating fracture healing under the condition of TBI and contributes to endochondral bone repair.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23349789</pmid><doi>10.1371/journal.pone.0054077</doi><tpages>e54077</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1327799267 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Antibodies Antibodies, Neutralizing - immunology Antibodies, Neutralizing - pharmacology Biology Bone growth Bone healing Bone histomorphometry Bone marrow Bone surgery Brain Brain injuries Brain Injuries - genetics Brain Injuries - metabolism Cell migration Cell Movement - drug effects Cells, Cultured Chemokine CXCL12 - genetics Chemokine CXCL12 - immunology Chemokine CXCL12 - metabolism Chemokines Chemotaxis Chemotaxis - drug effects CXCR4 protein Endochondral bone Engineering Femur Femur - drug effects Femur - injuries Femur - metabolism Fracture Healing - drug effects Fracture Healing - genetics Fracture repair Fractures (Injuries) Gene Expression Growth factors Head injuries Healing Heart attacks Heterocyclic Compounds - pharmacology Immunohistochemistry In vivo methods and tests Medical research Medicine Mesenchymal stem cells Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - metabolism Mesenchyme Mice Mice, Inbred C57BL mRNA Orthopedics Osteogenesis Polymerase chain reaction Receptors, CXCR4 - antagonists & inhibitors Receptors, CXCR4 - genetics Receptors, CXCR4 - metabolism Recombinant Proteins - pharmacology Repair Researchers Reverse Transcriptase Polymerase Chain Reaction Ribonucleic acid RNA Rodents SDF-1 protein Stem cells Studies Time Factors Traumatic brain injury |
| title | SDF-1 promotes endochondral bone repair during fracture healing at the traumatic brain injury condition |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T17%3A15%3A43IST&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=SDF-1%20promotes%20endochondral%20bone%20repair%20during%20fracture%20healing%20at%20the%20traumatic%20brain%20injury%20condition&rft.jtitle=PloS%20one&rft.au=Liu,%20Xiaoqi&rft.date=2013-01-22&rft.volume=8&rft.issue=1&rft.spage=e54077&rft.epage=e54077&rft.pages=e54077-e54077&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0054077&rft_dat=%3Cgale_plos_%3EA478167103%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=1327799267&rft_id=info:pmid/23349789&rft_galeid=A478167103&rft_doaj_id=oai_doaj_org_article_cda8567593824261997c4da83071ddd6&rfr_iscdi=true |