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CL Grosskreutz, VA Luukkaa, MB Pantcheva, NR Poulin; Activation of Caspase 9 in a Rat Model of Experimental Glaucoma . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4058.
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Purpose: We investigated the activation of caspase 9, a marker of the intrinsic caspase cascade, in the retinas of rats with experimentally-induced increased intraocular pressure (IOP). Methods:Elevated IOP was induced in rats by injecting 1.9 M sodium chloride into episcleral veins of a rat's left eye (OS) with the fellow eye (OD) serving as a control. Following elevation of IOP to various levels for at least 4 days, animals were sacrificed and the eyes removed and prepared for isolation of retinal proteins or immunohistochemistry. Procaspase 9 expression and the presence of activated caspase 9 (p35) were studied by immunohistochemistry and immunoblot analysis. Immunoblots were analyzed by densitometry and alpha-tubulin was used as a loading control. Intensity of IOP elevation was calculated as the area under the pressure-time curve divided by the number of days of IOP elevation. The levels of procaspase 9 were calculated as the ratio of experimental glaucoma eye to control eye (OS/OD). Results:The range of peak IOP in the experimental eyes was 22 to 42 mm Hg. By immunoblot anaysis, there was a positive correlation between total procaspase 9 (OS/OD) and intensity of IOP elevation. Cleaved caspase 9 (p35) bands were detected by immunoblot only in rats with peak IOP above 35 mm Hg for more than 4 days. Cleaved caspase 9 staining was seen only in the ganglion cell layer of retinas from rats with peak IOP greater than 32 mm Hg. Conclusion: These results support activation of caspase 9, the intrinsic caspase cascade in RGC death in experimental glaucoma.
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