| Budget Amount *help |
¥16,410,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2007: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2006: ¥10,300,000 (Direct Cost: ¥10,300,000)
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| Research Abstract |
During these two years, we proceeded for elucidating and creating new treatment for chorioretinal diseases. First, we confirmed that complement factor H Y402H polymorphism was related to the onset of age-related macular degeneration (AMD) and polypoidal choroidal vasculopathy (PCV), and Creactive protein (CRP)l levels were significantly higher in the participants with AMD and PCV (Ophthalmology, 2007). Then we identified that single nucleotide polymorphism in the promoter of HTRA1 and LOC387715 were related to the onset of AMD and PCV. Furthermore, the individuals with the risk allele of promoter of HTRA1 and LOC387715 showed the increase levels of CRP level, which indicated AMD and PCV were closely related to the inflammations (ARVO, 2008) .On the other hand, the patient with AMD and PCV who received photodynamic therapy (PDT) showed transient decrease of retinal function caused by the reduced chorioretinal circulation (IOVS, 2007). However, the combination therapy with PDT and pharma
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ceutical enabled to prevent the reduced macular function, and intravitreous injection of anti-angiogenic drugs increased macular function (ARVO, 2008)
Second, the collaborative research with Nagoya University, School of Engineering aimed for the treatment of AMD with autologous transplantation of retinal pigment epithelium. We identified efficient uptake of magnetic particles into ARPE19 cells and accelerated cell incorporation of plasmid. Moreover, we confirmed that magnetic cells could be guided using magnet in vitro (ARVO,2008) .
In the research on inherited diseases, we studied precisely the genotypic and phenotypic features of autosomal dominant optic atrophy (ADOA ; Ophthalmology,2006) .In this research, we detected the abnormality of inner retina using electroretinograms and optical coherence tomography (IOVS, 2007) .
In the basic research using animals, we found the existence of germinal zone capable of photoreceptor regeneration in the mouse ciliary body (IOVS, 2007). In addition, the photoreceptors of rd1 mice which has genetically progressed photoreceptor degeneration could be preserved with injection of vascular endothelial growth factor (VEGF; IOVS, 2007) and retinal detachment (IOVS, 2008). Moreover, we succeeded the first creation of middle-sized animal as, a model of retinitis pigmentosa. We induced the rhodopsin mutation (Pro347Leu)into the rabbit and created transgenic rabbit which has genetic photoreceptor degeneration. We confirmed progressive photoreceptor degeneration in this model using histological and electrophysiological analysis (ARVO, 2008). Less
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