| Project/Area Number |
15591882
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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 | Fukuoka University |
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Principal Investigator |
HAYASHI Hideyuki Fukuoka University, School of Medicine, Professor, 医学部, 教授 (30173024)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | thorombospondin / Vitamin A deficiency / cornea / neoangiogenesis / 創傷治癒 / トロンボスポンジン-1 / 細胞外マトリックス |
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| Research Abstract |
Vitamin A has been known to be necessary for maintaining epithelial cells in skin, mucosa, cornea and retina. vitamin A defect induces corneal epithelial defect, delayed wound healing in corneal epithelium and neovascularization in the cornea. Thus, a question raised that vitamin A may have bifacet action to maitain epithelia and inhibit angiogenesis. Therefore, we investigated the role of vitamin A.
Production of intrinsic anti-angiogenic molecules as thrombospondin(TSP) and pigment epithelium-derived factor(PEDF) by retinal pigment epithelial(RPE) cells was positively stimulated by vitamin A(retinoic acid). TSP molecules is produced and secreted by RPE cells, and accumulated on Bruch's membrane ; basement membrane of RPE cells on physiological retina. In experimental neovascularization in mouse choroid, defect of TSP accumulation was observed at the point neovascular blood vessels penetrate Bruch's membrane. Delayed corneal epithelial wound healing was observed on vitamin A deficient mice as TSP knocked out mice, and defective accumulation of TSP on wounded cornea was observed, and extrinsic TSP antagonistically encouraged epithelial healing. Vitamin A has biological role to maitain epithelium and inhibit angiogenesis.
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