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T. S. Rex, K. Kodali, Y. Wong, S. Merry; Erythropoietin Blocks Photoreceptor Apoptosis in the rds Mouse Model of Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2009;50(13):695.
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Previously, we demonstrated that systemic, but not intraocular, delivery of erythropoietin (EPO) by somatic gene therapy was neuroprotective to the photoreceptors. The goal of this study was to determine if this neuroprotection was due to EPO or to increased erythropoiesis.
Retinal degeneration slow (rds) mice were given a single subretinal injection of PBS, or 10U EPO, deglycosylated EPO, or hyperglycosylated EPO at postnatal day 7. Rescue was assessed by TUNEL analysis at postnatal day 20. TUNEL+ cells were quantified in representative sections through the eye. Hematocrit levels were measured by capillary centrifugation.
We detected 36 (±7; n=10) TUNEL + cells/mm retina in untreated rds retinas as compared to 5 (±6; n=12) TUNEL + cells/mm retina in EPO treated rds retinas. Retinas treated with deglycosylated or hyperglycosylated forms of EPO had 7 (±2.5; n=8), and 3 (±3; n=5), TUNEL+ cells/mm retina, respectively. PBS injected rds retinas contained 16 (±4; n=4) TUNEL + cells/mm retina. The percent hematocrit was unchanged between treated and untreated mice.
EPO is neuroprotective to the photoreceptors in the rds mouse by a direct effect in the retina, not via a secondary effect from increased oxygen availability because of increased erythropoiesis. And, lack of neuroprotection from ocular gene delivery is probably not due to insufficient glycosylation of EPO.
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