Nuclear fibroblast growth factor 2 (FGF2) isoforms inhibit bone marrow stromal cell mineralization through FGF23/FGFR/MAPK in vitro
Fibroblast growth factor 23 (FGF23) is responsible for phosphate wasting and the phenotypic changes observed in human diseases such as X‐linked hypophosphatemia (XLH). Targeted overexpression of nuclear high–molecular weight fibroblast growth factor 2 isoforms (HMW isoforms) in osteoblasts resulted...
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| Veröffentlicht in: | Journal of bone and mineral research 2013-01, Vol.28 (1), p.35-45 |
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| description | Fibroblast growth factor 23 (FGF23) is responsible for phosphate wasting and the phenotypic changes observed in human diseases such as X‐linked hypophosphatemia (XLH). Targeted overexpression of nuclear high–molecular weight fibroblast growth factor 2 isoforms (HMW isoforms) in osteoblasts resulted in a transgenic mouse with phenotypic changes similar to XLH, including increased FGF23, hypophosphatemia, and rickets/osteomalacia. The goal of this study was to assess whether HMW isoforms also reduced mineralized bone formation via phosphate‐independent effects in bone marrow stromal cells (BMSCs) by modulating FGF23/FGF receptor (FGFR)/extracellular signal‐regulated kinase (ERK) signaling. To determine if decreased bone formation in BMSC cultures from HMW transgenic mice could be rescued by blocking this pathway, an FGF23 neutralizing antibody, the FGFR tyrosine kinase inhibitor SU5402 and the mitogen‐activated protein kinase (MAPK) inhibitor PD98059 were used. FGF23 levels in the conditioned medium of HMW BMSC cultures were dramatically increased compared to BMSC from control (Vector) mice. Mineralized nodule formation was significantly decreased in HMW BMSC cultures compared with control cultures. The decreased nodule formation in HMW cultures was partially rescued by the FGF23 neutralizing antibody, SU5402 and PD98059. mRNA levels for the osteoblast‐related genes, osteocalcin, Runt‐related transcription factor 2 (Runx2), and osterix, and the osteocyte‐related gene dentin matrix acidic phosphoprotein 1 (Dmp1) were significantly decreased in HMW cultures compared with control cultures, and the decreases were partially rescued by SU5402 or PD98059 treatment. Matrix‐gla‐protein (Mgp) mRNA was significantly higher in HMW cultures compared with control cultures, reduced by SU5402, but further increased by PD98059. Our results suggest that phosphate‐independent effects of HMW isoforms in vitro may be directly mediated in part via FGF23 and that HMW isoforms signal via FGF23/FGFR/MAPK to inhibit bone formation in vitro. © 2013 American Society for Bone and Mineral Research |
| doi_str_mv | 10.1002/jbmr.1721 |
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Targeted overexpression of nuclear high–molecular weight fibroblast growth factor 2 isoforms (HMW isoforms) in osteoblasts resulted in a transgenic mouse with phenotypic changes similar to XLH, including increased FGF23, hypophosphatemia, and rickets/osteomalacia. The goal of this study was to assess whether HMW isoforms also reduced mineralized bone formation via phosphate‐independent effects in bone marrow stromal cells (BMSCs) by modulating FGF23/FGF receptor (FGFR)/extracellular signal‐regulated kinase (ERK) signaling. To determine if decreased bone formation in BMSC cultures from HMW transgenic mice could be rescued by blocking this pathway, an FGF23 neutralizing antibody, the FGFR tyrosine kinase inhibitor SU5402 and the mitogen‐activated protein kinase (MAPK) inhibitor PD98059 were used. FGF23 levels in the conditioned medium of HMW BMSC cultures were dramatically increased compared to BMSC from control (Vector) mice. Mineralized nodule formation was significantly decreased in HMW BMSC cultures compared with control cultures. The decreased nodule formation in HMW cultures was partially rescued by the FGF23 neutralizing antibody, SU5402 and PD98059. mRNA levels for the osteoblast‐related genes, osteocalcin, Runt‐related transcription factor 2 (Runx2), and osterix, and the osteocyte‐related gene dentin matrix acidic phosphoprotein 1 (Dmp1) were significantly decreased in HMW cultures compared with control cultures, and the decreases were partially rescued by SU5402 or PD98059 treatment. Matrix‐gla‐protein (Mgp) mRNA was significantly higher in HMW cultures compared with control cultures, reduced by SU5402, but further increased by PD98059. Our results suggest that phosphate‐independent effects of HMW isoforms in vitro may be directly mediated in part via FGF23 and that HMW isoforms signal via FGF23/FGFR/MAPK to inhibit bone formation in vitro. © 2013 American Society for Bone and Mineral Research</description><identifier>ISSN: 0884-0431</identifier><identifier>EISSN: 1523-4681</identifier><identifier>DOI: 10.1002/jbmr.1721</identifier><identifier>PMID: 22836867</identifier><identifier>CODEN: JBMREJ</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Antibodies ; Bone marrow ; Calcification, Physiologic - drug effects ; Cbfa-1 protein ; Cell culture ; Cell Nucleus - drug effects ; Cell Nucleus - metabolism ; Culture Media, Conditioned - pharmacology ; Extracellular signal-regulated kinase ; FGF RECEPTOR INHIBITOR ; FGF23 ; Fibroblast growth factor ; Fibroblast growth factor 2 ; Fibroblast Growth Factor 2 - genetics ; Fibroblast Growth Factor 2 - metabolism ; Fibroblast growth factor 23 ; Fibroblast growth factor receptors ; Fibroblast Growth Factors - genetics ; Fibroblast Growth Factors - metabolism ; Flavonoids - pharmacology ; Gene Expression Regulation - drug effects ; Genetic Vectors ; HMWFGF2 ; Humans ; Hypophosphatemia ; Male ; MAP kinase ; MAPK ; Mesenchymal Stromal Cells - drug effects ; Mesenchymal Stromal Cells - enzymology ; Mesenchymal Stromal Cells - metabolism ; Mice ; Mice, Transgenic ; Mineralization ; Mitogen-Activated Protein Kinases - metabolism ; Models, Biological ; Molecular Weight ; Neutralization Tests ; Nodules ; Osteocalcin ; Osteocalcin - genetics ; Osteocalcin - metabolism ; Osteogenesis ; Osteogenesis - drug effects ; Osteogenesis - genetics ; PHOSPHATE ; Phosphorylation - drug effects ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Pyrroles - pharmacology ; Receptors, Fibroblast Growth Factor - genetics ; Receptors, Fibroblast Growth Factor - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; stromal cells ; Time Factors ; Transcription factors ; Transgenic mice ; X chromosome</subject><ispartof>Journal of bone and mineral research, 2013-01, Vol.28 (1), p.35-45</ispartof><rights>Copyright © 2013 American Society for Bone and Mineral Research</rights><rights>Copyright © 2013 American Society for Bone and Mineral Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4871-da79a59956af07fdf962c46f895ddadb740e5ad27f0838ad37e8179d24128d483</citedby><cites>FETCH-LOGICAL-c4871-da79a59956af07fdf962c46f895ddadb740e5ad27f0838ad37e8179d24128d483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbmr.1721$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbmr.1721$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27933,27934,45583,45584</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22836867$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Liping</creatorcontrib><creatorcontrib>Esliger, Alycia</creatorcontrib><creatorcontrib>Hurley, Marja M</creatorcontrib><title>Nuclear fibroblast growth factor 2 (FGF2) isoforms inhibit bone marrow stromal cell mineralization through FGF23/FGFR/MAPK in vitro</title><title>Journal of bone and mineral research</title><addtitle>J Bone Miner Res</addtitle><description>Fibroblast growth factor 23 (FGF23) is responsible for phosphate wasting and the phenotypic changes observed in human diseases such as X‐linked hypophosphatemia (XLH). Targeted overexpression of nuclear high–molecular weight fibroblast growth factor 2 isoforms (HMW isoforms) in osteoblasts resulted in a transgenic mouse with phenotypic changes similar to XLH, including increased FGF23, hypophosphatemia, and rickets/osteomalacia. The goal of this study was to assess whether HMW isoforms also reduced mineralized bone formation via phosphate‐independent effects in bone marrow stromal cells (BMSCs) by modulating FGF23/FGF receptor (FGFR)/extracellular signal‐regulated kinase (ERK) signaling. To determine if decreased bone formation in BMSC cultures from HMW transgenic mice could be rescued by blocking this pathway, an FGF23 neutralizing antibody, the FGFR tyrosine kinase inhibitor SU5402 and the mitogen‐activated protein kinase (MAPK) inhibitor PD98059 were used. FGF23 levels in the conditioned medium of HMW BMSC cultures were dramatically increased compared to BMSC from control (Vector) mice. Mineralized nodule formation was significantly decreased in HMW BMSC cultures compared with control cultures. The decreased nodule formation in HMW cultures was partially rescued by the FGF23 neutralizing antibody, SU5402 and PD98059. mRNA levels for the osteoblast‐related genes, osteocalcin, Runt‐related transcription factor 2 (Runx2), and osterix, and the osteocyte‐related gene dentin matrix acidic phosphoprotein 1 (Dmp1) were significantly decreased in HMW cultures compared with control cultures, and the decreases were partially rescued by SU5402 or PD98059 treatment. Matrix‐gla‐protein (Mgp) mRNA was significantly higher in HMW cultures compared with control cultures, reduced by SU5402, but further increased by PD98059. Our results suggest that phosphate‐independent effects of HMW isoforms in vitro may be directly mediated in part via FGF23 and that HMW isoforms signal via FGF23/FGFR/MAPK to inhibit bone formation in vitro. © 2013 American Society for Bone and Mineral Research</description><subject>Animals</subject><subject>Antibodies</subject><subject>Bone marrow</subject><subject>Calcification, Physiologic - drug effects</subject><subject>Cbfa-1 protein</subject><subject>Cell culture</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - metabolism</subject><subject>Culture Media, Conditioned - pharmacology</subject><subject>Extracellular signal-regulated kinase</subject><subject>FGF RECEPTOR INHIBITOR</subject><subject>FGF23</subject><subject>Fibroblast growth factor</subject><subject>Fibroblast growth factor 2</subject><subject>Fibroblast Growth Factor 2 - genetics</subject><subject>Fibroblast Growth Factor 2 - metabolism</subject><subject>Fibroblast growth factor 23</subject><subject>Fibroblast growth factor receptors</subject><subject>Fibroblast Growth Factors - genetics</subject><subject>Fibroblast Growth Factors - metabolism</subject><subject>Flavonoids - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genetic Vectors</subject><subject>HMWFGF2</subject><subject>Humans</subject><subject>Hypophosphatemia</subject><subject>Male</subject><subject>MAP kinase</subject><subject>MAPK</subject><subject>Mesenchymal Stromal Cells - drug effects</subject><subject>Mesenchymal Stromal Cells - enzymology</subject><subject>Mesenchymal Stromal Cells - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mineralization</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Models, Biological</subject><subject>Molecular Weight</subject><subject>Neutralization Tests</subject><subject>Nodules</subject><subject>Osteocalcin</subject><subject>Osteocalcin - genetics</subject><subject>Osteocalcin - metabolism</subject><subject>Osteogenesis</subject><subject>Osteogenesis - drug effects</subject><subject>Osteogenesis - genetics</subject><subject>PHOSPHATE</subject><subject>Phosphorylation - drug effects</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Pyrroles - pharmacology</subject><subject>Receptors, Fibroblast Growth Factor - genetics</subject><subject>Receptors, Fibroblast Growth Factor - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>stromal cells</subject><subject>Time Factors</subject><subject>Transcription factors</subject><subject>Transgenic mice</subject><subject>X chromosome</subject><issn>0884-0431</issn><issn>1523-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10ctO3DAUBmALUZUpsOgLVJbYwCKM73aWgBjachWCdeTENuNREoOdFMGWF6_ToSwqdXO8-fzr6PwAfMXoECNE5qu6i4dYErwBZpgTWjCh8CaYIaVYgRjFW-BLSiuEkOBCfAZbhCgqlJAz8HY1Nq3VETpfx1C3Og3wIYbnYQmdboYQIYH7i7MFOYA-BRdil6Dvl772A6xDb2GnY-YwDTF0uoWNbVvY-d5G3fpXPfjQw2EZw_iwhFMMned5O788ujnPOfCXz_92wCen22R3399tcL84vTv5Xlxcn_04ObooGqYkLoyWpeZlyYV2SDrjSkEaJpwquTHa1JIhy7Uh0iFFlTZUWoVlaQjDRBmm6DbYX-c-xvA02jRUnU_Twrq3YUxVZhyVFHGe6d4_dBXG2OftsqKlFEJRltXBWjUxpBStqx6jzwd5qTCqpmaqqZlqaibbb--JY91Z8yH_VpHBfA2efWtf_p9U_Ty-vP0T-RveqpdU</recordid><startdate>201301</startdate><enddate>201301</enddate><creator>Xiao, Liping</creator><creator>Esliger, Alycia</creator><creator>Hurley, Marja M</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>7TS</scope><scope>K9.</scope></search><sort><creationdate>201301</creationdate><title>Nuclear fibroblast growth factor 2 (FGF2) isoforms inhibit bone marrow stromal cell mineralization through FGF23/FGFR/MAPK in vitro</title><author>Xiao, Liping ; Esliger, Alycia ; Hurley, Marja M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4871-da79a59956af07fdf962c46f895ddadb740e5ad27f0838ad37e8179d24128d483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Bone marrow</topic><topic>Calcification, Physiologic - drug effects</topic><topic>Cbfa-1 protein</topic><topic>Cell culture</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - metabolism</topic><topic>Culture Media, Conditioned - pharmacology</topic><topic>Extracellular signal-regulated kinase</topic><topic>FGF RECEPTOR INHIBITOR</topic><topic>FGF23</topic><topic>Fibroblast growth factor</topic><topic>Fibroblast growth factor 2</topic><topic>Fibroblast Growth Factor 2 - genetics</topic><topic>Fibroblast Growth Factor 2 - metabolism</topic><topic>Fibroblast growth factor 23</topic><topic>Fibroblast growth factor receptors</topic><topic>Fibroblast Growth Factors - genetics</topic><topic>Fibroblast Growth Factors - metabolism</topic><topic>Flavonoids - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genetic Vectors</topic><topic>HMWFGF2</topic><topic>Humans</topic><topic>Hypophosphatemia</topic><topic>Male</topic><topic>MAP kinase</topic><topic>MAPK</topic><topic>Mesenchymal Stromal Cells - drug effects</topic><topic>Mesenchymal Stromal Cells - enzymology</topic><topic>Mesenchymal Stromal Cells - metabolism</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mineralization</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Models, Biological</topic><topic>Molecular Weight</topic><topic>Neutralization Tests</topic><topic>Nodules</topic><topic>Osteocalcin</topic><topic>Osteocalcin - genetics</topic><topic>Osteocalcin - metabolism</topic><topic>Osteogenesis</topic><topic>Osteogenesis - drug effects</topic><topic>Osteogenesis - genetics</topic><topic>PHOSPHATE</topic><topic>Phosphorylation - drug effects</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Pyrroles - pharmacology</topic><topic>Receptors, Fibroblast Growth Factor - genetics</topic><topic>Receptors, Fibroblast Growth Factor - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>stromal cells</topic><topic>Time Factors</topic><topic>Transcription factors</topic><topic>Transgenic mice</topic><topic>X chromosome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Liping</creatorcontrib><creatorcontrib>Esliger, Alycia</creatorcontrib><creatorcontrib>Hurley, Marja M</creatorcontrib><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>Physical Education Index</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Journal of bone and mineral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Liping</au><au>Esliger, Alycia</au><au>Hurley, Marja M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nuclear fibroblast growth factor 2 (FGF2) isoforms inhibit bone marrow stromal cell mineralization through FGF23/FGFR/MAPK in vitro</atitle><jtitle>Journal of bone and mineral research</jtitle><addtitle>J Bone Miner Res</addtitle><date>2013-01</date><risdate>2013</risdate><volume>28</volume><issue>1</issue><spage>35</spage><epage>45</epage><pages>35-45</pages><issn>0884-0431</issn><eissn>1523-4681</eissn><coden>JBMREJ</coden><abstract>Fibroblast growth factor 23 (FGF23) is responsible for phosphate wasting and the phenotypic changes observed in human diseases such as X‐linked hypophosphatemia (XLH). Targeted overexpression of nuclear high–molecular weight fibroblast growth factor 2 isoforms (HMW isoforms) in osteoblasts resulted in a transgenic mouse with phenotypic changes similar to XLH, including increased FGF23, hypophosphatemia, and rickets/osteomalacia. The goal of this study was to assess whether HMW isoforms also reduced mineralized bone formation via phosphate‐independent effects in bone marrow stromal cells (BMSCs) by modulating FGF23/FGF receptor (FGFR)/extracellular signal‐regulated kinase (ERK) signaling. To determine if decreased bone formation in BMSC cultures from HMW transgenic mice could be rescued by blocking this pathway, an FGF23 neutralizing antibody, the FGFR tyrosine kinase inhibitor SU5402 and the mitogen‐activated protein kinase (MAPK) inhibitor PD98059 were used. FGF23 levels in the conditioned medium of HMW BMSC cultures were dramatically increased compared to BMSC from control (Vector) mice. Mineralized nodule formation was significantly decreased in HMW BMSC cultures compared with control cultures. The decreased nodule formation in HMW cultures was partially rescued by the FGF23 neutralizing antibody, SU5402 and PD98059. mRNA levels for the osteoblast‐related genes, osteocalcin, Runt‐related transcription factor 2 (Runx2), and osterix, and the osteocyte‐related gene dentin matrix acidic phosphoprotein 1 (Dmp1) were significantly decreased in HMW cultures compared with control cultures, and the decreases were partially rescued by SU5402 or PD98059 treatment. Matrix‐gla‐protein (Mgp) mRNA was significantly higher in HMW cultures compared with control cultures, reduced by SU5402, but further increased by PD98059. Our results suggest that phosphate‐independent effects of HMW isoforms in vitro may be directly mediated in part via FGF23 and that HMW isoforms signal via FGF23/FGFR/MAPK to inhibit bone formation in vitro. © 2013 American Society for Bone and Mineral Research</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22836867</pmid><doi>10.1002/jbmr.1721</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Bone marrow Calcification, Physiologic - drug effects Cbfa-1 protein Cell culture Cell Nucleus - drug effects Cell Nucleus - metabolism Culture Media, Conditioned - pharmacology Extracellular signal-regulated kinase FGF RECEPTOR INHIBITOR FGF23 Fibroblast growth factor Fibroblast growth factor 2 Fibroblast Growth Factor 2 - genetics Fibroblast Growth Factor 2 - metabolism Fibroblast growth factor 23 Fibroblast growth factor receptors Fibroblast Growth Factors - genetics Fibroblast Growth Factors - metabolism Flavonoids - pharmacology Gene Expression Regulation - drug effects Genetic Vectors HMWFGF2 Humans Hypophosphatemia Male MAP kinase MAPK Mesenchymal Stromal Cells - drug effects Mesenchymal Stromal Cells - enzymology Mesenchymal Stromal Cells - metabolism Mice Mice, Transgenic Mineralization Mitogen-Activated Protein Kinases - metabolism Models, Biological Molecular Weight Neutralization Tests Nodules Osteocalcin Osteocalcin - genetics Osteocalcin - metabolism Osteogenesis Osteogenesis - drug effects Osteogenesis - genetics PHOSPHATE Phosphorylation - drug effects Protein Isoforms - genetics Protein Isoforms - metabolism Pyrroles - pharmacology Receptors, Fibroblast Growth Factor - genetics Receptors, Fibroblast Growth Factor - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism stromal cells Time Factors Transcription factors Transgenic mice X chromosome |
| title | Nuclear fibroblast growth factor 2 (FGF2) isoforms inhibit bone marrow stromal cell mineralization through FGF23/FGFR/MAPK in vitro |
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