Source:http://linkedlifedata.com/resource/pubmed/id/18794121
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
18
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pubmed:dateCreated |
2008-9-16
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pubmed:abstractText |
Several lines of evidence indicate that Flt-1, a fms-like tyrosine kinase receptor, which binds to vascular endothelial growth factor (VEGF)-A, VEGF-B, and PlGF, is a positive regulator of angiogenesis in the context of tumor growth and metastasis. However, the molecular basis of its action is still not clear. Besides endothelial cells, Flt-1 is also expressed by other different cell types, including myeloid hematopoeitic cells (monocytes and macrophages). To examine the functions of Flt-1 expressed by bone marrow-derived myeloid cells in supporting tumor growth and angiogenesis, Flt-1 tyrosine kinase-deficient (Flt-1 TK-/-) bone marrow cells were transplanted into lethally irradiated syngeneic recipients. After hematopoietic reconstitution, we orthotopically implanted syngeneic wild-type glioma cells or glioma cells overexpressing either VEGF(164) or PlGF-2. Loss of Flt-1 signaling in bone marrow-derived myeloid cells led to a significant decrease in tumor volume and vascularization in gliomas. VEGF but not PlGF overexpressed by glioma cells restored the tumor growth rate in Flt-1 TK-/- bone marrow chimera. VEGF and PlGF overexpression by tumor cells induced an accumulation of bone marrow-derived myeloid cells into tumor tissue. This infiltration was decreased in tumors grown in Flt-1 TK-/- bone marrow chimeras. When investigating chemokines and growth factors involved in myeloid cell recruitment, we determined elevated SDF-1/CXCL12 levels in VEGF- and PlGF-overexpressing tumors. Collectively, these results suggest that Flt-1 signaling in myeloid cells is essential to amplify the angiogenic response and to promote glioma growth.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL12,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl12 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Flt1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Pigf protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor...
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1538-7445
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pubmed:author |
pubmed-author:HeilMatthiasM,
pubmed-author:JugoldManfredM,
pubmed-author:KerberMarkM,
pubmed-author:KiesslingFabianF,
pubmed-author:MacheinMarcia ReginaMR,
pubmed-author:PlateKarl HKH,
pubmed-author:ReissYvonneY,
pubmed-author:ShibuyaMasabumiM,
pubmed-author:TchaikovskiVadimV,
pubmed-author:WaltenbergerJohannesJ,
pubmed-author:WickersheimAnkeA
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7342-51
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18794121-Animals,
pubmed-meshheading:18794121-Bone Marrow Cells,
pubmed-meshheading:18794121-Capillary Permeability,
pubmed-meshheading:18794121-Cell Growth Processes,
pubmed-meshheading:18794121-Chemokine CXCL12,
pubmed-meshheading:18794121-Chimera,
pubmed-meshheading:18794121-Glioma,
pubmed-meshheading:18794121-Macrophages,
pubmed-meshheading:18794121-Mice,
pubmed-meshheading:18794121-Mice, Inbred C57BL,
pubmed-meshheading:18794121-Mice, Transgenic,
pubmed-meshheading:18794121-Myeloid Cells,
pubmed-meshheading:18794121-Neovascularization, Pathologic,
pubmed-meshheading:18794121-Proteins,
pubmed-meshheading:18794121-Signal Transduction,
pubmed-meshheading:18794121-Transfection,
pubmed-meshheading:18794121-Vascular Endothelial Growth Factor A,
pubmed-meshheading:18794121-Vascular Endothelial Growth Factor Receptor-1
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pubmed:year |
2008
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pubmed:articleTitle |
Flt-1 signaling in macrophages promotes glioma growth in vivo.
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pubmed:affiliation |
Tumor Angiogenesis Research Group, Department of Neurosurgery, University of Freiburg, Freiburg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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