Perturbations in Bone Formation and Resorption in Insulin‐Like Growth Factor Binding Protein‐3 Transgenic Mice
IGF‐I and their binding proteins are important in bone health. Examination of BMD, osteoblast proliferation, and markers of bone resorption in transgenic mice that constitutively overexpress IGFBP‐3 indicates that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs ost...
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| creator | Silha, Josef V Mishra, Suresh Rosen, Clifford J Beamer, Wesley G Turner, Russell T Powell, David R Murphy, Liam J |
| description | IGF‐I and their binding proteins are important in bone health. Examination of BMD, osteoblast proliferation, and markers of bone resorption in transgenic mice that constitutively overexpress IGFBP‐3 indicates that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.
Introduction: Low serum insulin‐like growth factor I (IGF‐I) levels correlate with an increased risk of osteoporotic fractures. Serum IGF‐I is largely bound to IGF‐binding protein‐3 (IGFBP‐3), which can inhibit IGF‐I action and enhance delivery of IGF‐I to tissues. Its role in bone biology is unclear.
Methods: Bone mineral density (BMD), osteoblast proliferation, and markers of bone resorption were examined in transgenic (Tg) mice that constitutively overexpressed human IGFBP‐3 cDNA driven by either the cytomegalovirus (CMV) or phosphoglycerate kinase (PGK) promoter.
Results: Cultured calvarial osteoblasts from Tg mice expressed the transgene and grew more slowly than cells from wild‐type (Wt) mice, and the mitogenic response to IGF‐I was attenuated in osteoblasts from Tg mice. Total volumetric BMD and cortical BMD, measured in the femur using peripheral quantitative computed tomography (pQCT) were significantly reduced in both Tg mouse strains compared with Wt mice. PGKBP‐3 Tg mice showed the most marked reduction in bone density. Osteocalcin levels were similar in Wt and CMVBP‐3 Tg mice but were significantly reduced in PGKBP‐3 Tg mice. Urinary deoxypyridinoline and osteoclast perimeter, markers of bone resorption, were significantly increased in both Tg mouse strains compared with Wt mice. Using double labeling with tetracycline, we demonstrated that pericortical and endocortical mineral apposition rate was significantly reduced in PGKBP‐3 Tg mice compared with Wt mice.
Conclusions: These data show that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation. |
| doi_str_mv | 10.1359/jbmr.2003.18.10.1834 |
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Introduction: Low serum insulin‐like growth factor I (IGF‐I) levels correlate with an increased risk of osteoporotic fractures. Serum IGF‐I is largely bound to IGF‐binding protein‐3 (IGFBP‐3), which can inhibit IGF‐I action and enhance delivery of IGF‐I to tissues. Its role in bone biology is unclear.
Methods: Bone mineral density (BMD), osteoblast proliferation, and markers of bone resorption were examined in transgenic (Tg) mice that constitutively overexpressed human IGFBP‐3 cDNA driven by either the cytomegalovirus (CMV) or phosphoglycerate kinase (PGK) promoter.
Results: Cultured calvarial osteoblasts from Tg mice expressed the transgene and grew more slowly than cells from wild‐type (Wt) mice, and the mitogenic response to IGF‐I was attenuated in osteoblasts from Tg mice. Total volumetric BMD and cortical BMD, measured in the femur using peripheral quantitative computed tomography (pQCT) were significantly reduced in both Tg mouse strains compared with Wt mice. PGKBP‐3 Tg mice showed the most marked reduction in bone density. Osteocalcin levels were similar in Wt and CMVBP‐3 Tg mice but were significantly reduced in PGKBP‐3 Tg mice. Urinary deoxypyridinoline and osteoclast perimeter, markers of bone resorption, were significantly increased in both Tg mouse strains compared with Wt mice. Using double labeling with tetracycline, we demonstrated that pericortical and endocortical mineral apposition rate was significantly reduced in PGKBP‐3 Tg mice compared with Wt mice.
Conclusions: These data show that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.</description><identifier>ISSN: 0884-0431</identifier><identifier>EISSN: 1523-4681</identifier><identifier>DOI: 10.1359/jbmr.2003.18.10.1834</identifier><identifier>PMID: 14584894</identifier><identifier>CODEN: JBMREJ</identifier><language>eng</language><publisher>Washington, DC: John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)</publisher><subject>Amino Acids - pharmacology ; Animals ; Biological and medical sciences ; Blotting, Western ; Bone and Bones - pathology ; Bone Density ; Cell Division ; Coloring Agents - pharmacology ; Cytomegalovirus - genetics ; Diseases of the osteoarticular system ; DNA, Complementary - metabolism ; Dose-Response Relationship, Drug ; Insulin-Like Growth Factor Binding Protein 3 - genetics ; Insulin-Like Growth Factor Binding Protein 3 - physiology ; Insulin-Like Growth Factor I - metabolism ; insulin‐like growth binding protein‐3 ; Medical sciences ; Mice ; Mice, Transgenic ; osteoblast ; Osteoblasts - cytology ; Osteoblasts - metabolism ; Osteocalcin - metabolism ; osteoclast ; Osteoporosis. Osteomalacia. Paget disease ; Phenotype ; Phosphoglycerate Kinase - genetics ; Promoter Regions, Genetic ; Tetrazolium Salts - pharmacology ; Thiazoles - pharmacology ; Time Factors ; transgenic mice</subject><ispartof>Journal of bone and mineral research, 2003-10, Vol.18 (10), p.1834-1841</ispartof><rights>Copyright © 2003 ASBMR</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4875-ed5e9859a372e6d651dce96629066da75c975be7794c797977af83698d9ec67d3</citedby><cites>FETCH-LOGICAL-c4875-ed5e9859a372e6d651dce96629066da75c975be7794c797977af83698d9ec67d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1359%2Fjbmr.2003.18.10.1834$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1359%2Fjbmr.2003.18.10.1834$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15200302$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14584894$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Silha, Josef V</creatorcontrib><creatorcontrib>Mishra, Suresh</creatorcontrib><creatorcontrib>Rosen, Clifford J</creatorcontrib><creatorcontrib>Beamer, Wesley G</creatorcontrib><creatorcontrib>Turner, Russell T</creatorcontrib><creatorcontrib>Powell, David R</creatorcontrib><creatorcontrib>Murphy, Liam J</creatorcontrib><title>Perturbations in Bone Formation and Resorption in Insulin‐Like Growth Factor Binding Protein‐3 Transgenic Mice</title><title>Journal of bone and mineral research</title><addtitle>J Bone Miner Res</addtitle><description>IGF‐I and their binding proteins are important in bone health. Examination of BMD, osteoblast proliferation, and markers of bone resorption in transgenic mice that constitutively overexpress IGFBP‐3 indicates that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.
Introduction: Low serum insulin‐like growth factor I (IGF‐I) levels correlate with an increased risk of osteoporotic fractures. Serum IGF‐I is largely bound to IGF‐binding protein‐3 (IGFBP‐3), which can inhibit IGF‐I action and enhance delivery of IGF‐I to tissues. Its role in bone biology is unclear.
Methods: Bone mineral density (BMD), osteoblast proliferation, and markers of bone resorption were examined in transgenic (Tg) mice that constitutively overexpressed human IGFBP‐3 cDNA driven by either the cytomegalovirus (CMV) or phosphoglycerate kinase (PGK) promoter.
Results: Cultured calvarial osteoblasts from Tg mice expressed the transgene and grew more slowly than cells from wild‐type (Wt) mice, and the mitogenic response to IGF‐I was attenuated in osteoblasts from Tg mice. Total volumetric BMD and cortical BMD, measured in the femur using peripheral quantitative computed tomography (pQCT) were significantly reduced in both Tg mouse strains compared with Wt mice. PGKBP‐3 Tg mice showed the most marked reduction in bone density. Osteocalcin levels were similar in Wt and CMVBP‐3 Tg mice but were significantly reduced in PGKBP‐3 Tg mice. Urinary deoxypyridinoline and osteoclast perimeter, markers of bone resorption, were significantly increased in both Tg mouse strains compared with Wt mice. Using double labeling with tetracycline, we demonstrated that pericortical and endocortical mineral apposition rate was significantly reduced in PGKBP‐3 Tg mice compared with Wt mice.
Conclusions: These data show that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.</description><subject>Amino Acids - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Bone and Bones - pathology</subject><subject>Bone Density</subject><subject>Cell Division</subject><subject>Coloring Agents - pharmacology</subject><subject>Cytomegalovirus - genetics</subject><subject>Diseases of the osteoarticular system</subject><subject>DNA, Complementary - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Insulin-Like Growth Factor Binding Protein 3 - genetics</subject><subject>Insulin-Like Growth Factor Binding Protein 3 - physiology</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>insulin‐like growth binding protein‐3</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>osteoblast</subject><subject>Osteoblasts - cytology</subject><subject>Osteoblasts - metabolism</subject><subject>Osteocalcin - metabolism</subject><subject>osteoclast</subject><subject>Osteoporosis. Osteomalacia. Paget disease</subject><subject>Phenotype</subject><subject>Phosphoglycerate Kinase - genetics</subject><subject>Promoter Regions, Genetic</subject><subject>Tetrazolium Salts - pharmacology</subject><subject>Thiazoles - pharmacology</subject><subject>Time Factors</subject><subject>transgenic mice</subject><issn>0884-0431</issn><issn>1523-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1uEzEUhS0EoqHwBgh5A7sJ9vh_B6ma_igVVVXWluO5KS4zdrBnVHXXR-AZeRJmkkhdgu7CukffOVfyQeg9JXPKhPl8v-7yvCaEzameT6Jm_AWaUVGziktNX6IZ0ZpXhDN6hN6Uck8IkULK1-iIcqG5NnyG8jXkfshr14cUCw4RL1IEvEy520nYxQbfQEl5u1tH4CKWoQ3xz9PvVfgJ-Cynh_4HXjrfp4wXITYh3uHrnHrYQQzfZhfLHcTg8VXw8Ba92ri2wLvDe4y-L09vT86r1bezi5Ovq8pzrUQFjQCjhXFM1SAbKWjjwUhZGyJl45TwRok1KGW4V2Yc5TaaSaMbA16qhh2jT_vcbU6_Bii97ULx0LYuQhqKVZTR0aX-CVJT15yKCeR70OdUSoaN3ebQufxoKbFTKXYqxU6lWKp34ljKaPtwyB_WHTTPpkMLI_DxALjiXbsZ_8uH8syJKZHUI_dlzz2EFh7_67i9XFzdCCkI1ZRQwf4CK8OrCA</recordid><startdate>200310</startdate><enddate>200310</enddate><creator>Silha, Josef V</creator><creator>Mishra, Suresh</creator><creator>Rosen, Clifford J</creator><creator>Beamer, Wesley G</creator><creator>Turner, Russell T</creator><creator>Powell, David R</creator><creator>Murphy, Liam J</creator><general>John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)</general><general>American Society for Bone and Mineral Research</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>7QP</scope><scope>7X8</scope></search><sort><creationdate>200310</creationdate><title>Perturbations in Bone Formation and Resorption in Insulin‐Like Growth Factor Binding Protein‐3 Transgenic Mice</title><author>Silha, Josef V ; Mishra, Suresh ; Rosen, Clifford J ; Beamer, Wesley G ; Turner, Russell T ; Powell, David R ; Murphy, Liam J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4875-ed5e9859a372e6d651dce96629066da75c975be7794c797977af83698d9ec67d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Amino Acids - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Bone and Bones - pathology</topic><topic>Bone Density</topic><topic>Cell Division</topic><topic>Coloring Agents - pharmacology</topic><topic>Cytomegalovirus - genetics</topic><topic>Diseases of the osteoarticular system</topic><topic>DNA, Complementary - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Insulin-Like Growth Factor Binding Protein 3 - genetics</topic><topic>Insulin-Like Growth Factor Binding Protein 3 - physiology</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>insulin‐like growth binding protein‐3</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>osteoblast</topic><topic>Osteoblasts - cytology</topic><topic>Osteoblasts - metabolism</topic><topic>Osteocalcin - metabolism</topic><topic>osteoclast</topic><topic>Osteoporosis. Osteomalacia. Paget disease</topic><topic>Phenotype</topic><topic>Phosphoglycerate Kinase - genetics</topic><topic>Promoter Regions, Genetic</topic><topic>Tetrazolium Salts - pharmacology</topic><topic>Thiazoles - pharmacology</topic><topic>Time Factors</topic><topic>transgenic mice</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Silha, Josef V</creatorcontrib><creatorcontrib>Mishra, Suresh</creatorcontrib><creatorcontrib>Rosen, Clifford J</creatorcontrib><creatorcontrib>Beamer, Wesley G</creatorcontrib><creatorcontrib>Turner, Russell T</creatorcontrib><creatorcontrib>Powell, David R</creatorcontrib><creatorcontrib>Murphy, Liam J</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>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bone and mineral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Silha, Josef V</au><au>Mishra, Suresh</au><au>Rosen, Clifford J</au><au>Beamer, Wesley G</au><au>Turner, Russell T</au><au>Powell, David R</au><au>Murphy, Liam J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Perturbations in Bone Formation and Resorption in Insulin‐Like Growth Factor Binding Protein‐3 Transgenic Mice</atitle><jtitle>Journal of bone and mineral research</jtitle><addtitle>J Bone Miner Res</addtitle><date>2003-10</date><risdate>2003</risdate><volume>18</volume><issue>10</issue><spage>1834</spage><epage>1841</epage><pages>1834-1841</pages><issn>0884-0431</issn><eissn>1523-4681</eissn><coden>JBMREJ</coden><abstract>IGF‐I and their binding proteins are important in bone health. Examination of BMD, osteoblast proliferation, and markers of bone resorption in transgenic mice that constitutively overexpress IGFBP‐3 indicates that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.
Introduction: Low serum insulin‐like growth factor I (IGF‐I) levels correlate with an increased risk of osteoporotic fractures. Serum IGF‐I is largely bound to IGF‐binding protein‐3 (IGFBP‐3), which can inhibit IGF‐I action and enhance delivery of IGF‐I to tissues. Its role in bone biology is unclear.
Methods: Bone mineral density (BMD), osteoblast proliferation, and markers of bone resorption were examined in transgenic (Tg) mice that constitutively overexpressed human IGFBP‐3 cDNA driven by either the cytomegalovirus (CMV) or phosphoglycerate kinase (PGK) promoter.
Results: Cultured calvarial osteoblasts from Tg mice expressed the transgene and grew more slowly than cells from wild‐type (Wt) mice, and the mitogenic response to IGF‐I was attenuated in osteoblasts from Tg mice. Total volumetric BMD and cortical BMD, measured in the femur using peripheral quantitative computed tomography (pQCT) were significantly reduced in both Tg mouse strains compared with Wt mice. PGKBP‐3 Tg mice showed the most marked reduction in bone density. Osteocalcin levels were similar in Wt and CMVBP‐3 Tg mice but were significantly reduced in PGKBP‐3 Tg mice. Urinary deoxypyridinoline and osteoclast perimeter, markers of bone resorption, were significantly increased in both Tg mouse strains compared with Wt mice. Using double labeling with tetracycline, we demonstrated that pericortical and endocortical mineral apposition rate was significantly reduced in PGKBP‐3 Tg mice compared with Wt mice.
Conclusions: These data show that overexpression of IGFBP‐3 increases osteoclast number and bone resorption, impairs osteoblast proliferation, and has a significant negative effect on bone formation.</abstract><cop>Washington, DC</cop><pub>John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)</pub><pmid>14584894</pmid><doi>10.1359/jbmr.2003.18.10.1834</doi><tpages>8</tpages></addata></record> |
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| subjects | Amino Acids - pharmacology Animals Biological and medical sciences Blotting, Western Bone and Bones - pathology Bone Density Cell Division Coloring Agents - pharmacology Cytomegalovirus - genetics Diseases of the osteoarticular system DNA, Complementary - metabolism Dose-Response Relationship, Drug Insulin-Like Growth Factor Binding Protein 3 - genetics Insulin-Like Growth Factor Binding Protein 3 - physiology Insulin-Like Growth Factor I - metabolism insulin‐like growth binding protein‐3 Medical sciences Mice Mice, Transgenic osteoblast Osteoblasts - cytology Osteoblasts - metabolism Osteocalcin - metabolism osteoclast Osteoporosis. Osteomalacia. Paget disease Phenotype Phosphoglycerate Kinase - genetics Promoter Regions, Genetic Tetrazolium Salts - pharmacology Thiazoles - pharmacology Time Factors transgenic mice |
| title | Perturbations in Bone Formation and Resorption in Insulin‐Like Growth Factor Binding Protein‐3 Transgenic Mice |
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