| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
We evaluated the protective effect of midkine (MK), the product of a retinoic acid responsive gene, on ischemia-reperfusion injured retinal degeneration in the rats. MK or buffer controls were injected intravitreally two days before ischemia reperfusion injury. After 7 or 14 days of ischemic damage, the eyes were perfused with a fixative, bisected along the vertical meridian, embedded in plastic and then sectioned. The degree of retinal ischemic damage was assessed for plastic-embedded sections by cytological analysis, measuring the thickness of several layrs and by counting the numbers of the ganglion cells. Seven and 14 days after ischemia-reperfusion injury, the retinas of uninjected controls and those of rats injected with phosphate buffered saline (PBS) showed a decrease in the thickness and a reduction in the cell numbers in inner retinal layrs. The photoreceptor layr and outer nuclear layr appeared almost normal. The retinas of MK-injected eyes were found to be transiently rescued or protected from ischemic damage. It was very hard to get such amount of MK from L-cell system, therefore Kaneda et al. produced a recombinant basulovirus clone which expresses a large amount of mouse MK in the culture medium than L-cell. We evaluated the survival promoting activity of each midkine produced by L-cell system, baculo virus system in the constant light-induced photoreceptor degeneration of the rat. Also, Rat pleiotrophin (PTN,known as heparin-binding growth-associated molecule) was examined in light damaged model of the rat. MK from L-cell appeared a little higher score than MK from baculovirus The eyes injected with PTN had a low score.
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