Effect of VEGF's on osteockast formation and activation

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Vascular endothelial growth factor (VEGF) is a key mediator of physiological angiogenesis. This cytokine binds to two cell surface receptors which are encoded by flt-1 or flk-1/KDR that also belong to the tyrosine kinase receptor family. Only the Flt-1 is expressed on macrophage monocyte lineage. In the present study, we investigated that whether the effect of VEGF treatment on the osteoclast differentiation in vitro. Bone marrow cells and spleen cells were obtained from 5-to 8-week-old male ddy miceor op/op mice. Non adherent G10-passed cells were cultured in & alpha-MEM with 15% FBS, 100 ng/ml RANKL, 20 ng/ml GSF-1 or 100 ng/ml VEGF. After culture for 7 days, smaller size of TRAP positive multinucleated cells were observed in the presence of RANKL and VEGF from bone marrow cells and spleen cells(Wt & op), as well as resorption pits were found than that of in the presence of RANKL and CSF-1. Treatment with Flt-1/Fc chimera, and anti VEGF antibody inhibit the RANKL and VEGF-induced osteoclast differentiation but neutralizing anti-CSF-1 Receptor antibody did not. In addition, Flt-1 was detected by immunocytochemical study with anti-Flt-1 antibody but not Flk-1 on osteoclast and its precursors. These results suggest that VEGF has important role in osteoclast differentiation and bone resorption system as well as CSF-1.