STUDY ON THE EFFECTS OF ENDOTHELIAL GROWTH FCTOR ON BONE METABOLISM
| Project/Area Number |
12671772
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
NIIDA Shumpei Hiroshima University, Faculty of Dentistry, Research Associate, 歯学部, 助手 (10137630)
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| Co-Investigator(Kenkyū-buntansha) |
MAEDA Norihiko Hiroshima University, Faculty of Dentistry, Professor, 歯学部, 教授 (60049418)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | osteoclast / op / op mouse / VEGF / M-CSF / estrogen |
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| Research Abstract |
Recently, we found that vascular endothelial growth factor (VEGF) can substitute for macrophage colony-stimulating factor (M-CSF), which is an essential factor for osteoclastogenesis. In the present study, we elucidated that the morphology of the osteoclasts induced by VEGF and the effects of VGEF on activity of mature osteoclsts. In addition, we assessed the effects of VEGF on osteoclastogenesis under the condition of estrogen deficiency caused by ovariectmy (OVX).
A single injection of the recombinant human (rh) VEGF (5μg) into osteopetrotic (op/op) mice induced many osteoclasts in the bone. Although, osteoclast induced by rhVEGF was small cell including a few nuclei, the well-developed ruffled border membrane and clear zones were observed electron microscopically. Next, we examined the effects of VEGF on activity of mature osteoclasts in vitro. The rhVEGF also affects cell spreading and morphological changes in mature osteoclasts. These results suggest the VEGF stimulates bone resorbing activity of osteoclasts. On the other hand, the number of osteoclasts increased significantly in OVX-op/op mice, and this phenomenon was inhibited by VEGF antagonistic treatment, Flt-1/Fc chimeric protein. These results suggested that estrogen regulates VEGF function for osteoclastogenesis as well as M-CSF.
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Report
(3 results)
Research Products
(7 results)
