Vav3 regulates osteoclast function and bone mass
Osteoporosis, a leading cause of morbidity in the elderly, is characterized by progressive loss of bone mass resulting from excess osteoclastic bone resorption relative to osteoblastic bone formation. Here we identify Vav3, a Rho family guanine nucleotide exchange factor, as essential for stimulated...
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Veröffentlicht in: | Nature medicine 2005-03, Vol.11 (3), p.284-290 |
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creator | Ross, F Patrick Swat, Wojciech Faccio, Roberta Teitelbaum, Steven L Fujikawa, Keiko Chappel, Jean Zallone, Alberta Tybulewicz, Victor L |
description | Osteoporosis, a leading cause of morbidity in the elderly, is characterized by progressive loss of bone mass resulting from excess osteoclastic bone resorption relative to osteoblastic bone formation. Here we identify Vav3, a Rho family guanine nucleotide exchange factor, as essential for stimulated osteoclast activation and bone density
in vivo
. Vav3-deficient osteoclasts show defective actin cytoskeleton organization, polarization, spreading and resorptive activity resulting from impaired signaling downstream of the M-CSF receptor and α
v
β
3
integrin. Vav3-deficient mice have increased bone mass and are protected from bone loss induced by systemic bone resorption stimuli such as parathyroid hormone or RANKL. Moreover, we provide genetic and biochemical evidence for the role of Syk tyrosine kinase as a crucial upstream regulator of Vav3 in osteoclasts. Thus, Vav3 is a potential new target for antiosteoporosis therapy. |
doi_str_mv | 10.1038/nm1194 |
format | Article |
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in vivo
. Vav3-deficient osteoclasts show defective actin cytoskeleton organization, polarization, spreading and resorptive activity resulting from impaired signaling downstream of the M-CSF receptor and α
v
β
3
integrin. Vav3-deficient mice have increased bone mass and are protected from bone loss induced by systemic bone resorption stimuli such as parathyroid hormone or RANKL. Moreover, we provide genetic and biochemical evidence for the role of Syk tyrosine kinase as a crucial upstream regulator of Vav3 in osteoclasts. Thus, Vav3 is a potential new target for antiosteoporosis therapy.</description><identifier>ISSN: 1078-8956</identifier><identifier>EISSN: 1546-170X</identifier><identifier>DOI: 10.1038/nm1194</identifier><identifier>PMID: 15711558</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Bone Density ; Bone Resorption - physiopathology ; Bone surgery ; Cancer Research ; Carrier Proteins - pharmacology ; Cell Cycle Proteins - biosynthesis ; Cell Cycle Proteins - physiology ; Cytoskeleton ; Guanine Nucleotide Exchange Factors - physiology ; Infectious Diseases ; Integrin alphaVbeta3 - physiology ; Kinases ; Macrophage Colony-Stimulating Factor - pharmacology ; Membrane Glycoproteins - pharmacology ; Metabolic Diseases ; Mice ; Molecular Medicine ; Morbidity ; Neurosciences ; Osteoclasts - drug effects ; Osteoclasts - pathology ; Osteoclasts - physiology ; Osteoporosis ; Protein-Tyrosine Kinases - physiology ; Proteins ; Proto-Oncogene Proteins - biosynthesis ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-vav ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; Rho Factor - physiology ; Signal transduction ; Upstream ; ZAP-70 Protein-Tyrosine Kinase</subject><ispartof>Nature medicine, 2005-03, Vol.11 (3), p.284-290</ispartof><rights>Springer Nature America, Inc. 2005</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Mar 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c564t-3465c9f764607a8c270e96e95ef95cfd1672fb1052a798317da301e265df916d3</citedby><cites>FETCH-LOGICAL-c564t-3465c9f764607a8c270e96e95ef95cfd1672fb1052a798317da301e265df916d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2727,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15711558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ross, F Patrick</creatorcontrib><creatorcontrib>Swat, Wojciech</creatorcontrib><creatorcontrib>Faccio, Roberta</creatorcontrib><creatorcontrib>Teitelbaum, Steven L</creatorcontrib><creatorcontrib>Fujikawa, Keiko</creatorcontrib><creatorcontrib>Chappel, Jean</creatorcontrib><creatorcontrib>Zallone, Alberta</creatorcontrib><creatorcontrib>Tybulewicz, Victor L</creatorcontrib><title>Vav3 regulates osteoclast function and bone mass</title><title>Nature medicine</title><addtitle>Nat Med</addtitle><addtitle>Nat Med</addtitle><description>Osteoporosis, a leading cause of morbidity in the elderly, is characterized by progressive loss of bone mass resulting from excess osteoclastic bone resorption relative to osteoblastic bone formation. Here we identify Vav3, a Rho family guanine nucleotide exchange factor, as essential for stimulated osteoclast activation and bone density
in vivo
. Vav3-deficient osteoclasts show defective actin cytoskeleton organization, polarization, spreading and resorptive activity resulting from impaired signaling downstream of the M-CSF receptor and α
v
β
3
integrin. Vav3-deficient mice have increased bone mass and are protected from bone loss induced by systemic bone resorption stimuli such as parathyroid hormone or RANKL. Moreover, we provide genetic and biochemical evidence for the role of Syk tyrosine kinase as a crucial upstream regulator of Vav3 in osteoclasts. Thus, Vav3 is a potential new target for antiosteoporosis therapy.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bone Density</subject><subject>Bone Resorption - physiopathology</subject><subject>Bone surgery</subject><subject>Cancer Research</subject><subject>Carrier Proteins - pharmacology</subject><subject>Cell Cycle Proteins - biosynthesis</subject><subject>Cell Cycle Proteins - physiology</subject><subject>Cytoskeleton</subject><subject>Guanine Nucleotide Exchange Factors - physiology</subject><subject>Infectious Diseases</subject><subject>Integrin alphaVbeta3 - physiology</subject><subject>Kinases</subject><subject>Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Membrane Glycoproteins - pharmacology</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Molecular Medicine</subject><subject>Morbidity</subject><subject>Neurosciences</subject><subject>Osteoclasts - drug effects</subject><subject>Osteoclasts - pathology</subject><subject>Osteoclasts - physiology</subject><subject>Osteoporosis</subject><subject>Protein-Tyrosine Kinases - physiology</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-vav</subject><subject>RANK Ligand</subject><subject>Receptor Activator of Nuclear Factor-kappa B</subject><subject>Rho Factor - physiology</subject><subject>Signal transduction</subject><subject>Upstream</subject><subject>ZAP-70 Protein-Tyrosine Kinase</subject><issn>1078-8956</issn><issn>1546-170X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0t1r1TAUAPAiiptT_wKR4sOGD505SZM0j2O4DxgM_Bi-ldz0pOtok5mkov-9ufSyOXdByUNC8ss55OQUxWsgh0BY88FNAKp-UuwCr0UFknx7mtdENlWjuNgpXsR4QwhhhKvnxQ5wCcB5s1uQK_2DlQH7edQJY-ljQm9GHVNpZ2fS4F2pXVeuvMNy0jG-LJ5ZPUZ8tZn3iq8nH78cn1UXl6fnx0cXleGiThWrBTfKSlELInVjqCSoBCqOVnFjOxCS2hUQTrVUDQPZaUYAqeCdVSA6tlfsL3Fvg_8-Y0ztNESD46gd-jm2QtZNTkL-CUEySkCpDN_9BW_8HFx-REspAwq1EBlVC-r1iO3grE9Bmx4dBj3mGtghbx-BooIKxdbZD7f4PDqcBrP1wvsHF7JJ-DP1eo6xPf_86f_t5dVDu_-HvUY9puvox3n9g3ErNMHHGNC2t2GYdPjVAmnXvdQuvZTh20295tWE3T3bNE8GBwuI-cj1GO4L-ijUm0U6neaAd6E2x78BcRDURQ</recordid><startdate>20050301</startdate><enddate>20050301</enddate><creator>Ross, F Patrick</creator><creator>Swat, Wojciech</creator><creator>Faccio, Roberta</creator><creator>Teitelbaum, Steven L</creator><creator>Fujikawa, Keiko</creator><creator>Chappel, Jean</creator><creator>Zallone, Alberta</creator><creator>Tybulewicz, Victor L</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050301</creationdate><title>Vav3 regulates osteoclast function and bone mass</title><author>Ross, F Patrick ; Swat, Wojciech ; Faccio, Roberta ; Teitelbaum, Steven L ; Fujikawa, Keiko ; Chappel, Jean ; Zallone, Alberta ; Tybulewicz, Victor L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c564t-3465c9f764607a8c270e96e95ef95cfd1672fb1052a798317da301e265df916d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bone Density</topic><topic>Bone Resorption - 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Academic</collection><jtitle>Nature medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ross, F Patrick</au><au>Swat, Wojciech</au><au>Faccio, Roberta</au><au>Teitelbaum, Steven L</au><au>Fujikawa, Keiko</au><au>Chappel, Jean</au><au>Zallone, Alberta</au><au>Tybulewicz, Victor L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vav3 regulates osteoclast function and bone mass</atitle><jtitle>Nature medicine</jtitle><stitle>Nat Med</stitle><addtitle>Nat Med</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>11</volume><issue>3</issue><spage>284</spage><epage>290</epage><pages>284-290</pages><issn>1078-8956</issn><eissn>1546-170X</eissn><abstract>Osteoporosis, a leading cause of morbidity in the elderly, is characterized by progressive loss of bone mass resulting from excess osteoclastic bone resorption relative to osteoblastic bone formation. Here we identify Vav3, a Rho family guanine nucleotide exchange factor, as essential for stimulated osteoclast activation and bone density
in vivo
. Vav3-deficient osteoclasts show defective actin cytoskeleton organization, polarization, spreading and resorptive activity resulting from impaired signaling downstream of the M-CSF receptor and α
v
β
3
integrin. Vav3-deficient mice have increased bone mass and are protected from bone loss induced by systemic bone resorption stimuli such as parathyroid hormone or RANKL. Moreover, we provide genetic and biochemical evidence for the role of Syk tyrosine kinase as a crucial upstream regulator of Vav3 in osteoclasts. Thus, Vav3 is a potential new target for antiosteoporosis therapy.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>15711558</pmid><doi>10.1038/nm1194</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Biomedical and Life Sciences Biomedicine Bone Density Bone Resorption - physiopathology Bone surgery Cancer Research Carrier Proteins - pharmacology Cell Cycle Proteins - biosynthesis Cell Cycle Proteins - physiology Cytoskeleton Guanine Nucleotide Exchange Factors - physiology Infectious Diseases Integrin alphaVbeta3 - physiology Kinases Macrophage Colony-Stimulating Factor - pharmacology Membrane Glycoproteins - pharmacology Metabolic Diseases Mice Molecular Medicine Morbidity Neurosciences Osteoclasts - drug effects Osteoclasts - pathology Osteoclasts - physiology Osteoporosis Protein-Tyrosine Kinases - physiology Proteins Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-vav RANK Ligand Receptor Activator of Nuclear Factor-kappa B Rho Factor - physiology Signal transduction Upstream ZAP-70 Protein-Tyrosine Kinase |
title | Vav3 regulates osteoclast function and bone mass |
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