| Summary: | 碩士 === 國立中山大學 === 生物科學系研究所 === 95 === Age-related macular degeneration (ARMD) is the leading cause for visual impairment and blindness in the elder population of developed countries. The primary underlying cause for significant visual loss is the choroidal neovascularization (CNV). CNV is also generated in high myopia ; angioid streaks and some inflammatory diseases and rarely after laser photocoagulation. Current treatment strategies for ARMD include laser photocoagulation , photodynamic therapy , but neither treatment addresses underlying stimuli for blood vessel growth. Therefore, recurrent disease is a problem of clinical significant relevance. Surgical excision of submacular neovascular membrane lead to the additional damage of the retinal pigment epithelium (RPE). Consequently, use of therapeutic agents that directly inhibit the angiogenic stimuli may be able to provide a more effective and permanent treatment. Vasostatin (VS) , the N-terminal domain (amino acid 1-180) of a calcium-binding protein , is a potent angiogenesis inhibitor , isolated from culture supernatants of an Epstein-Barr virus-immortalized cell line. In previous studies, we demonstrated that gene delivery of angiogenesis inhibitor vasostatin attenuated the corneal neovascularization in animals. The recombinant vasostatin also prevented or apparently reduced growth of human Burkitt lymphoma and human colon carcinoma in animal model. The primary objective of this study was to vasostatin attenuated the choroidal neovascularization in animals. Retinal and visual function will be evaluated.
The above experiments would enable us to test the hypothesis that the topical application of VS delivery might be a promising strategy for the treatment of ARMD and other retinal disorders. Furthermore, the results from animal studies might be extrapolated for future clinical application.
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