Impaired fracture healing in macrophage migration inhibitory factor-deficient mice
Summary This study investigated the role of macrophage migration inhibitory factor (MIF) in fracture repair using MIF gene-deficient mice (MIF KO). Fracture healing was delayed in MIF KO, and this was mainly due to the delay in the mineralization of osteoid within the fracture callus. Introduction W...
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| Veröffentlicht in: | Osteoporosis international 2011-06, Vol.22 (6), p.1955-1965 |
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| container_title | Osteoporosis international |
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| creator | Kobayashi, T. Onodera, S. Kondo, E. Tohyama, H. Fujiki, H. Yokoyama, A. Yasuda, K. |
| description | Summary
This study investigated the role of macrophage migration inhibitory factor (MIF) in fracture repair using MIF gene-deficient mice (MIF KO). Fracture healing was delayed in MIF KO, and this was mainly due to the delay in the mineralization of osteoid within the fracture callus.
Introduction
We previously reported that the expression of macrophage migration inhibitory factor (MIF) was up-regulated during the fracture healing process in rats. However, its role in the pathophysiology of this process remained unclear. The aim of the present study was to clarify the role of MIF in the fracture healing process using MIF gene-deficient mice (MIF KO).
Methods
Bone repair in wild-type mice (WT) and MIF KO (
n
= 70, respectively) was investigated using a tibia fracture model. Radiographic, biomechanical, histological, bone histomorphometric, and molecular analyses were performed.
Results
Post-fracture biomechanical testing showed that maximum load and stiffness were significantly lower in MIF KO than in WT on day 42. However, similar levels were observed between the two groups on day 84. Bone histomorphometric analysis revealed significantly higher osteoid volume, a lower mineral apposition rate, and smaller numbers of osteoclasts in the MIF KO callus compared to the WT callus. The messenger ribonucleic acid expressions of matrix metalloproteinase (MMP)-2, membranous type 1-MMP, cathepsin K, and tissue nonspecific alkaline phosphatase were found to be significantly suppressed in the MIF KO callus.
Conclusion
The results of the present study suggest that delayed fracture healing in MIF KO was mainly attributable to a delay in osteoid mineralization. |
| doi_str_mv | 10.1007/s00198-010-1385-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_876226577</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>876226577</sourcerecordid><originalsourceid>FETCH-LOGICAL-c498t-eefa138bf6bb9901c294f2469e35e89dfa50a2443f184a37514a5fad5ea1597b3</originalsourceid><addsrcrecordid>eNqFkV1LHDEUhkOp1K3tD-hNGQriVTSfk-RSRK0gCGKhd8OZzMluZD7WZObCf98su61QKL0KyXne95yTl5AvnJ1zxsxFZow7SxlnlEurKXtHVlxJSYWr9XuyYk4a6hT_eUw-5vzMisY584EcC2alNbVdkce7YQsxYVeFBH5eElYbhD6O6yqO1QA-TdsNrLEa4jrBHKexvG9iG-cpvVahSKZEOwzRRxznQnn8RI4C9Bk_H84T8uPm-unqO71_uL27urynXjk7U8QAZeo21G3rHONeOBWEqh1KjdZ1ATQDoZQM3CqQRnMFOkCnEbh2ppUn5Gzvu03Ty4J5boaYPfY9jDgtuSkLClFrY_5P1rWWQjpZyG9_kc_TksayRrHTWjql6wLxPVQ-J-eEodmmOEB6bThrdsE0-2AatruXYBpWNF8Pxks7YPdH8TuJApweAMge-pLG6GN-4xS3WpgdJ_ZcLqVxjeltwn93_wUdFaVR</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>875539456</pqid></control><display><type>article</type><title>Impaired fracture healing in macrophage migration inhibitory factor-deficient mice</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Kobayashi, T. ; Onodera, S. ; Kondo, E. ; Tohyama, H. ; Fujiki, H. ; Yokoyama, A. ; Yasuda, K.</creator><creatorcontrib>Kobayashi, T. ; Onodera, S. ; Kondo, E. ; Tohyama, H. ; Fujiki, H. ; Yokoyama, A. ; Yasuda, K.</creatorcontrib><description>Summary
This study investigated the role of macrophage migration inhibitory factor (MIF) in fracture repair using MIF gene-deficient mice (MIF KO). Fracture healing was delayed in MIF KO, and this was mainly due to the delay in the mineralization of osteoid within the fracture callus.
Introduction
We previously reported that the expression of macrophage migration inhibitory factor (MIF) was up-regulated during the fracture healing process in rats. However, its role in the pathophysiology of this process remained unclear. The aim of the present study was to clarify the role of MIF in the fracture healing process using MIF gene-deficient mice (MIF KO).
Methods
Bone repair in wild-type mice (WT) and MIF KO (
n
= 70, respectively) was investigated using a tibia fracture model. Radiographic, biomechanical, histological, bone histomorphometric, and molecular analyses were performed.
Results
Post-fracture biomechanical testing showed that maximum load and stiffness were significantly lower in MIF KO than in WT on day 42. However, similar levels were observed between the two groups on day 84. Bone histomorphometric analysis revealed significantly higher osteoid volume, a lower mineral apposition rate, and smaller numbers of osteoclasts in the MIF KO callus compared to the WT callus. The messenger ribonucleic acid expressions of matrix metalloproteinase (MMP)-2, membranous type 1-MMP, cathepsin K, and tissue nonspecific alkaline phosphatase were found to be significantly suppressed in the MIF KO callus.
Conclusion
The results of the present study suggest that delayed fracture healing in MIF KO was mainly attributable to a delay in osteoid mineralization.</description><identifier>ISSN: 0937-941X</identifier><identifier>EISSN: 1433-2965</identifier><identifier>DOI: 10.1007/s00198-010-1385-0</identifier><identifier>PMID: 20838768</identifier><language>eng</language><publisher>London: Springer-Verlag</publisher><subject>Alkaline Phosphatase - biosynthesis ; Alkaline Phosphatase - genetics ; Animals ; Biological and medical sciences ; Bone Remodeling - physiology ; Bones ; Bony Callus - pathology ; Bony Callus - physiopathology ; Calcification, Physiologic - physiology ; Cathepsin K - biosynthesis ; Cathepsin K - genetics ; Cell physiology ; Diseases of the osteoarticular system ; Endocrinology ; Fracture Fixation, Intramedullary - methods ; Fracture Healing - physiology ; Fractures ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation ; Genetics ; Injuries of the limb. Injuries of the spine ; Intramolecular Oxidoreductases - deficiency ; Intramolecular Oxidoreductases - physiology ; Macrophage Migration-Inhibitory Factors - deficiency ; Macrophage Migration-Inhibitory Factors - physiology ; Male ; Matrix Metalloproteinase 1 - biosynthesis ; Matrix Metalloproteinase 1 - genetics ; Matrix Metalloproteinase 2 - biosynthesis ; Matrix Metalloproteinase 2 - genetics ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mineralization, calcification ; Molecular and cellular biology ; Original Article ; Orthopedics ; Osteoporosis. Osteomalacia. Paget disease ; Radiography ; Real-Time Polymerase Chain Reaction - methods ; Rheumatology ; RNA, Messenger - genetics ; Rodents ; Stress, Mechanical ; Tibial Fractures - diagnostic imaging ; Tibial Fractures - pathology ; Tibial Fractures - physiopathology ; Tibial Fractures - surgery ; Traumas. Diseases due to physical agents ; Wound healing</subject><ispartof>Osteoporosis international, 2011-06, Vol.22 (6), p.1955-1965</ispartof><rights>International Osteoporosis Foundation and National Osteoporosis Foundation 2010</rights><rights>2015 INIST-CNRS</rights><rights>International Osteoporosis Foundation and National Osteoporosis Foundation 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c498t-eefa138bf6bb9901c294f2469e35e89dfa50a2443f184a37514a5fad5ea1597b3</citedby><cites>FETCH-LOGICAL-c498t-eefa138bf6bb9901c294f2469e35e89dfa50a2443f184a37514a5fad5ea1597b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00198-010-1385-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00198-010-1385-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24185278$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20838768$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kobayashi, T.</creatorcontrib><creatorcontrib>Onodera, S.</creatorcontrib><creatorcontrib>Kondo, E.</creatorcontrib><creatorcontrib>Tohyama, H.</creatorcontrib><creatorcontrib>Fujiki, H.</creatorcontrib><creatorcontrib>Yokoyama, A.</creatorcontrib><creatorcontrib>Yasuda, K.</creatorcontrib><title>Impaired fracture healing in macrophage migration inhibitory factor-deficient mice</title><title>Osteoporosis international</title><addtitle>Osteoporos Int</addtitle><addtitle>Osteoporos Int</addtitle><description>Summary
This study investigated the role of macrophage migration inhibitory factor (MIF) in fracture repair using MIF gene-deficient mice (MIF KO). Fracture healing was delayed in MIF KO, and this was mainly due to the delay in the mineralization of osteoid within the fracture callus.
Introduction
We previously reported that the expression of macrophage migration inhibitory factor (MIF) was up-regulated during the fracture healing process in rats. However, its role in the pathophysiology of this process remained unclear. The aim of the present study was to clarify the role of MIF in the fracture healing process using MIF gene-deficient mice (MIF KO).
Methods
Bone repair in wild-type mice (WT) and MIF KO (
n
= 70, respectively) was investigated using a tibia fracture model. Radiographic, biomechanical, histological, bone histomorphometric, and molecular analyses were performed.
Results
Post-fracture biomechanical testing showed that maximum load and stiffness were significantly lower in MIF KO than in WT on day 42. However, similar levels were observed between the two groups on day 84. Bone histomorphometric analysis revealed significantly higher osteoid volume, a lower mineral apposition rate, and smaller numbers of osteoclasts in the MIF KO callus compared to the WT callus. The messenger ribonucleic acid expressions of matrix metalloproteinase (MMP)-2, membranous type 1-MMP, cathepsin K, and tissue nonspecific alkaline phosphatase were found to be significantly suppressed in the MIF KO callus.
Conclusion
The results of the present study suggest that delayed fracture healing in MIF KO was mainly attributable to a delay in osteoid mineralization.</description><subject>Alkaline Phosphatase - biosynthesis</subject><subject>Alkaline Phosphatase - genetics</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone Remodeling - physiology</subject><subject>Bones</subject><subject>Bony Callus - pathology</subject><subject>Bony Callus - physiopathology</subject><subject>Calcification, Physiologic - physiology</subject><subject>Cathepsin K - biosynthesis</subject><subject>Cathepsin K - genetics</subject><subject>Cell physiology</subject><subject>Diseases of the osteoarticular system</subject><subject>Endocrinology</subject><subject>Fracture Fixation, Intramedullary - methods</subject><subject>Fracture Healing - physiology</subject><subject>Fractures</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation</subject><subject>Genetics</subject><subject>Injuries of the limb. Injuries of the spine</subject><subject>Intramolecular Oxidoreductases - deficiency</subject><subject>Intramolecular Oxidoreductases - physiology</subject><subject>Macrophage Migration-Inhibitory Factors - deficiency</subject><subject>Macrophage Migration-Inhibitory Factors - physiology</subject><subject>Male</subject><subject>Matrix Metalloproteinase 1 - biosynthesis</subject><subject>Matrix Metalloproteinase 1 - genetics</subject><subject>Matrix Metalloproteinase 2 - biosynthesis</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Mineralization, calcification</subject><subject>Molecular and cellular biology</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Osteoporosis. Osteomalacia. Paget disease</subject><subject>Radiography</subject><subject>Real-Time Polymerase Chain Reaction - methods</subject><subject>Rheumatology</subject><subject>RNA, Messenger - genetics</subject><subject>Rodents</subject><subject>Stress, Mechanical</subject><subject>Tibial Fractures - diagnostic imaging</subject><subject>Tibial Fractures - pathology</subject><subject>Tibial Fractures - physiopathology</subject><subject>Tibial Fractures - surgery</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Wound healing</subject><issn>0937-941X</issn><issn>1433-2965</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkV1LHDEUhkOp1K3tD-hNGQriVTSfk-RSRK0gCGKhd8OZzMluZD7WZObCf98su61QKL0KyXne95yTl5AvnJ1zxsxFZow7SxlnlEurKXtHVlxJSYWr9XuyYk4a6hT_eUw-5vzMisY584EcC2alNbVdkce7YQsxYVeFBH5eElYbhD6O6yqO1QA-TdsNrLEa4jrBHKexvG9iG-cpvVahSKZEOwzRRxznQnn8RI4C9Bk_H84T8uPm-unqO71_uL27urynXjk7U8QAZeo21G3rHONeOBWEqh1KjdZ1ATQDoZQM3CqQRnMFOkCnEbh2ppUn5Gzvu03Ty4J5boaYPfY9jDgtuSkLClFrY_5P1rWWQjpZyG9_kc_TksayRrHTWjql6wLxPVQ-J-eEodmmOEB6bThrdsE0-2AatruXYBpWNF8Pxks7YPdH8TuJApweAMge-pLG6GN-4xS3WpgdJ_ZcLqVxjeltwn93_wUdFaVR</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Kobayashi, T.</creator><creator>Onodera, S.</creator><creator>Kondo, E.</creator><creator>Tohyama, H.</creator><creator>Fujiki, H.</creator><creator>Yokoyama, A.</creator><creator>Yasuda, K.</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20110601</creationdate><title>Impaired fracture healing in macrophage migration inhibitory factor-deficient mice</title><author>Kobayashi, T. ; Onodera, S. ; Kondo, E. ; Tohyama, H. ; Fujiki, H. ; Yokoyama, A. ; Yasuda, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-eefa138bf6bb9901c294f2469e35e89dfa50a2443f184a37514a5fad5ea1597b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Alkaline Phosphatase - biosynthesis</topic><topic>Alkaline Phosphatase - genetics</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone Remodeling - physiology</topic><topic>Bones</topic><topic>Bony Callus - pathology</topic><topic>Bony Callus - physiopathology</topic><topic>Calcification, Physiologic - physiology</topic><topic>Cathepsin K - biosynthesis</topic><topic>Cathepsin K - genetics</topic><topic>Cell physiology</topic><topic>Diseases of the osteoarticular system</topic><topic>Endocrinology</topic><topic>Fracture Fixation, Intramedullary - methods</topic><topic>Fracture Healing - physiology</topic><topic>Fractures</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation</topic><topic>Genetics</topic><topic>Injuries of the limb. Injuries of the spine</topic><topic>Intramolecular Oxidoreductases - deficiency</topic><topic>Intramolecular Oxidoreductases - physiology</topic><topic>Macrophage Migration-Inhibitory Factors - deficiency</topic><topic>Macrophage Migration-Inhibitory Factors - physiology</topic><topic>Male</topic><topic>Matrix Metalloproteinase 1 - biosynthesis</topic><topic>Matrix Metalloproteinase 1 - genetics</topic><topic>Matrix Metalloproteinase 2 - biosynthesis</topic><topic>Matrix Metalloproteinase 2 - genetics</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Mineralization, calcification</topic><topic>Molecular and cellular biology</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Osteoporosis. Osteomalacia. Paget disease</topic><topic>Radiography</topic><topic>Real-Time Polymerase Chain Reaction - methods</topic><topic>Rheumatology</topic><topic>RNA, Messenger - genetics</topic><topic>Rodents</topic><topic>Stress, Mechanical</topic><topic>Tibial Fractures - diagnostic imaging</topic><topic>Tibial Fractures - pathology</topic><topic>Tibial Fractures - physiopathology</topic><topic>Tibial Fractures - surgery</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kobayashi, T.</creatorcontrib><creatorcontrib>Onodera, S.</creatorcontrib><creatorcontrib>Kondo, E.</creatorcontrib><creatorcontrib>Tohyama, H.</creatorcontrib><creatorcontrib>Fujiki, H.</creatorcontrib><creatorcontrib>Yokoyama, A.</creatorcontrib><creatorcontrib>Yasuda, K.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Osteoporosis international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kobayashi, T.</au><au>Onodera, S.</au><au>Kondo, E.</au><au>Tohyama, H.</au><au>Fujiki, H.</au><au>Yokoyama, A.</au><au>Yasuda, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired fracture healing in macrophage migration inhibitory factor-deficient mice</atitle><jtitle>Osteoporosis international</jtitle><stitle>Osteoporos Int</stitle><addtitle>Osteoporos Int</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>22</volume><issue>6</issue><spage>1955</spage><epage>1965</epage><pages>1955-1965</pages><issn>0937-941X</issn><eissn>1433-2965</eissn><abstract>Summary
This study investigated the role of macrophage migration inhibitory factor (MIF) in fracture repair using MIF gene-deficient mice (MIF KO). Fracture healing was delayed in MIF KO, and this was mainly due to the delay in the mineralization of osteoid within the fracture callus.
Introduction
We previously reported that the expression of macrophage migration inhibitory factor (MIF) was up-regulated during the fracture healing process in rats. However, its role in the pathophysiology of this process remained unclear. The aim of the present study was to clarify the role of MIF in the fracture healing process using MIF gene-deficient mice (MIF KO).
Methods
Bone repair in wild-type mice (WT) and MIF KO (
n
= 70, respectively) was investigated using a tibia fracture model. Radiographic, biomechanical, histological, bone histomorphometric, and molecular analyses were performed.
Results
Post-fracture biomechanical testing showed that maximum load and stiffness were significantly lower in MIF KO than in WT on day 42. However, similar levels were observed between the two groups on day 84. Bone histomorphometric analysis revealed significantly higher osteoid volume, a lower mineral apposition rate, and smaller numbers of osteoclasts in the MIF KO callus compared to the WT callus. The messenger ribonucleic acid expressions of matrix metalloproteinase (MMP)-2, membranous type 1-MMP, cathepsin K, and tissue nonspecific alkaline phosphatase were found to be significantly suppressed in the MIF KO callus.
Conclusion
The results of the present study suggest that delayed fracture healing in MIF KO was mainly attributable to a delay in osteoid mineralization.</abstract><cop>London</cop><pub>Springer-Verlag</pub><pmid>20838768</pmid><doi>10.1007/s00198-010-1385-0</doi><tpages>11</tpages></addata></record> |
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| ispartof | Osteoporosis international, 2011-06, Vol.22 (6), p.1955-1965 |
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| language | eng |
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| subjects | Alkaline Phosphatase - biosynthesis Alkaline Phosphatase - genetics Animals Biological and medical sciences Bone Remodeling - physiology Bones Bony Callus - pathology Bony Callus - physiopathology Calcification, Physiologic - physiology Cathepsin K - biosynthesis Cathepsin K - genetics Cell physiology Diseases of the osteoarticular system Endocrinology Fracture Fixation, Intramedullary - methods Fracture Healing - physiology Fractures Fundamental and applied biological sciences. Psychology Gene Expression Regulation Genetics Injuries of the limb. Injuries of the spine Intramolecular Oxidoreductases - deficiency Intramolecular Oxidoreductases - physiology Macrophage Migration-Inhibitory Factors - deficiency Macrophage Migration-Inhibitory Factors - physiology Male Matrix Metalloproteinase 1 - biosynthesis Matrix Metalloproteinase 1 - genetics Matrix Metalloproteinase 2 - biosynthesis Matrix Metalloproteinase 2 - genetics Medical sciences Medicine Medicine & Public Health Mice Mice, Inbred BALB C Mice, Knockout Mineralization, calcification Molecular and cellular biology Original Article Orthopedics Osteoporosis. Osteomalacia. Paget disease Radiography Real-Time Polymerase Chain Reaction - methods Rheumatology RNA, Messenger - genetics Rodents Stress, Mechanical Tibial Fractures - diagnostic imaging Tibial Fractures - pathology Tibial Fractures - physiopathology Tibial Fractures - surgery Traumas. Diseases due to physical agents Wound healing |
| title | Impaired fracture healing in macrophage migration inhibitory factor-deficient mice |
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