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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1999-8-16
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pubmed:abstractText |
We demonstrated previously that a single injection of recombinant human macrophage colony-stimulating factor (rhM-CSF) is sufficient for osteoclast recruitment and survival in osteopetrotic (op/op) mice with a deficiency in osteoclasts resulting from a mutation in M-CSF gene. In this study, we show that a single injection of recombinant human vascular endothelial growth factor (rhVEGF) can similarly induce osteoclast recruitment in op/op mice. Osteoclasts predominantly expressed VEGF receptor 1 (VEGFR-1), and activity of recombinant human placenta growth factor 1 on osteoclast recruitment was comparable to that of rhVEGF, showing that the VEGF signal is mediated through VEGFR-1. The rhM-CSF-induced osteoclasts died after injections of VEGFR-1/Fc chimeric protein, and its effect was abrogated by concomitant injections of rhM-CSF. Osteoclasts supported by rhM-CSF or endogenous VEGF showed no significant difference in the bone-resorbing activity. op/op mice undergo an age-related resolution of osteopetrosis accompanied by an increase in osteoclast number. Most of the osteoclasts disappeared after injections of anti-VEGF antibody, demonstrating that endogenously produced VEGF is responsible for the appearance of osteoclasts in the mutant mice. In addition, rhVEGF replaced rhM-CSF in the support of in vitro osteoclast differentiation. These results demonstrate that M-CSF and VEGF have overlapping functions in the support of osteoclastic bone resorption.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-10027413,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-1262696,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-1409676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-1724107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-1915705,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-1985123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-2022928,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-2146111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-2188141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-2669999,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-3332553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-4610054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-7072615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-7130905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-7596436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-7742081,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-7795257,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-7929268,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8079662,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8137761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8418205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8545103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8602241,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8602242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8605350,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8663424,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-8822205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9202240,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9493833,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9520411,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9524283,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9568710,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9610749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9689083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10432291-9872925
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
190
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
293-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10432291-Animals,
pubmed-meshheading:10432291-Bone Resorption,
pubmed-meshheading:10432291-Cell Differentiation,
pubmed-meshheading:10432291-Cell Division,
pubmed-meshheading:10432291-Endothelial Growth Factors,
pubmed-meshheading:10432291-Humans,
pubmed-meshheading:10432291-Lymphokines,
pubmed-meshheading:10432291-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:10432291-Male,
pubmed-meshheading:10432291-Mice,
pubmed-meshheading:10432291-Mice, Mutant Strains,
pubmed-meshheading:10432291-Mutation,
pubmed-meshheading:10432291-Osteoclasts,
pubmed-meshheading:10432291-Osteopetrosis,
pubmed-meshheading:10432291-Recombinant Proteins,
pubmed-meshheading:10432291-Vascular Endothelial Growth Factor A,
pubmed-meshheading:10432291-Vascular Endothelial Growth Factors
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pubmed:year |
1999
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pubmed:articleTitle |
Vascular endothelial growth factor can substitute for macrophage colony-stimulating factor in the support of osteoclastic bone resorption.
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pubmed:affiliation |
Department of Anatomy, Hiroshima University School of Dentistry, Hiroshima 734-8553, Japan. sniida@ipc.hiroshima-u.ac.jp
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pubmed:publicationType |
Journal Article,
In Vitro
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