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J. Arai, N. Katai, K. Kuida, N. Yoshimura; Decreased Retinal Neuronal Apoptosis In Caspase–1 Deficient Mice . Invest. Ophthalmol. Vis. Sci. 2004;45(13):749.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To determine whether retinal neuronal apoptosis is altered in caspase–1 deficient mice after excessive light exposure and ischemia–reperfusion injury Methods: Eight to 10–week–old caspase–1 deficient mice (Casp1–/–) and wild–type (WT) mice were exposed to diffuse, cool, white fluorescent light of 25,000 lux for 2 hours. Other mice were subjected to retinal ischemia by increasing the intraocular pressure to 110 mmHg for 45 minutes. Electroretinograms (ERGs) were recorded before and after the light exposure. TdT–dUTP terminal nick–end labeling (TUNEL) was performed to identify the apoptotic cells after the insults. The inner retinal thickness was measured to evaluate the retinal injury after the ischemia–reperfusion. Expression of caspase–1 protein was studied by immunohistochemically and Western blotting. Results: After the light exposure, the amplitudes of the ERG a– and b–waves in Casp1–/– mice were significantly larger than those of the WT mice. The number of TUNEL–positive photoreceptor nuclei after the light exposure and the number of nuclei in the inner nuclear layer after the ischemia–reperfusion injury were significantly fewer in Casp1–/– mice than in the WT mice (p<0.001). There were more caspase–1–positive photoreceptor cells in WT mice after the light injury. 14 days after reperfusion, the retinal thickness of wild type and of ICE (–/–) were 29.6+/–6.4 micron and 35.5+/–8.9 micron, respectively (p < 0.05). Conclusions: Retinal neuronal apoptosis is much less prominent in Casp1–/– mice after excessive light exposure and ischemia–reperfusion injury. These data indicate that caspase–1 plays a role in retinal neuronal apoptosis.
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