2000 Fiscal Year Final Research Report Summary
RESEARCH ON PATHOGENESIS AND TREATMENT OF OCULAR VASCULAR DISEASES
| Project/Area Number |
09307040
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| Research Category |
Grant-in-Aid for Scientific Research (A).
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
INOMATA Hajime Graduate School of Medical Sciences KYUSHU UNIVERSITY Professor, 大学院・医学研究院, 教授 (30038674)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAMOTO Taiji Faculty of Medicine KYUSHU UNIVERSITY Assistant, 医学部・附属病院, 助手 (10235179)
ISHIBASHI Tatsuro Graduate School Medical Sciences KYUSHU UNIVERSITY Associate Professor, 大学院・医学研究院, 助教授 (30150428)
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| Project Period (FY) |
1997 – 2000
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| Keywords | Neovascularization / Malignant Melanoma / Adenovirus Vector / Subretinal Neovascularization / Wound Healing / Tissue Plasminogen Activator / Transforming Growth Factor-β / Vascular Endothelial Growth Factor |
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| Research Abstract |
We examined the effect of adenovirus-mediated gene transfer of a soluble receptor of vascular endothelial growth factor (VEGF) on the growth of experimental eyelid malignant melanoma, and it was found that the VEGF receptor (flt-1) gene inhibited the growth of the tumor. However, it caused the severe skin ulcer. Similarly, experimental subretinal neovascularization was inhibited by adenovirus-mediated soluble VEGF/flt-1 receptor gene transfection : as a role of VEGF and possible treatment for SRN in age-related macular degeneration. However, severe damages occurred in the sensory retina.
From these experimental studies, it became clear that neovascularization is rather important and indispensable phenomenon for wound healing of the tissues and organs. Therefore, it seems to be more important to inhibit the inflammation and/or tissue fibrosis during the wound healing.
To have the ideal wound healing, we prepared adenovirus vector to inhibit tissue plasminogen activator and transforming growth factor-β (TGF-β). Our results demonstrated that TGF-β indeed plays a critical role in the process of corneal opacification, edema and angiogenesis, and that adenovirus-mediated expression of a soluble TGF-β receptor can be therapeutically useful.
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