| Project/Area Number |
08672043
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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 |
Ophthalmology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
OGATA Nahoko Dep.Ophthalmology, Kansai Medical University Assistant Professor, 医学部, 講師 (60204062)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUSIMA Masashi Dep.of Ophthalmology, Kansai Medical University Assistant Professor, 医学部, 講師 (00192336)
NISHIMURA Tetsuya Department of Ophthalmology, Kansai Medical University Professor, 医学部, 助教授 (30156111)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | bFGF / TGFbeta / choroidal neovascularization / VEGF / HVJ-liposome method / gene therapy / retinal vein occlusion / transient retinal ischemis / 脈絡膜血管新生 |
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| Research Abstract |
We investigated mRNA expression of growth factors in laser induced experimental choroidal neovascularizon (CNV) in rats. Expression of basic fibroblast growth factor (bFGF) and its receptor, transforming growth factor (TGF) -beta (mainly TGF-beta2) mRNA and its reseptor was observed markedly in cells of neovascular lesions. Our findings indicated that endogenous bFGF and TGF-beta promotes CNV through autocrine and paracrine mechanism. Immunoreactivity for VEGF was markedly observed in CNV.This results was confirmed by RT-PCR and Western blotting. We revealed that macrophages is the mainsource of VEGF.
We successfully treated experimenral choroidal neovascularization with administration of TNP,interferon-beta, tecogalan.
We demonstrated that HVJ liposome method can transfer genes efficiently into choroidal neovascularization in a rat model. VEGF antisense oligonucleotides were specifically transferred into cells in the lesions of choroidal neovascularization. HVJ liposome method provides a highly efficient means of gene therapy for CNV.
We induced bFGF gene or bFGF antisense gene into cultured (RPE). These cell lines would be useful for the transplantation to treat CNV.
bFGF and its receptor mRNAs were expressed in the ischemic retina in a rat model of retinal vein occlusion, and bFGF and its receptor, midkine mRNAs were expressed in transient retinal ischemia induced by ocular pressure. These results suggest that ischemia regulates these factors.
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