Expression of p53 in Retina Neuronal Cell Death Induced by Ischemia and Reperfusion
Journal of the Korean Ophthalmological Society
; : 2679-2686, 1998.
Article
en Ko
| WPRIM
| ID: wpr-151812
Biblioteca responsable:
WPRO
ABSTRACT
In order to elucidate the mechanism of neuronal cell death induced by retina ischemia and reperfusion, we investigated expression of p53, Bcl-2, and ICE(interleukin converting enzyme) in retinal neuronal cell death. Adult male Spague-Dawley rats were used and their intraocular pressures were maintained between 160 and 180mmHg for 90 min to induce retina ischemia. Retinal cell death was observed by light microscopy from 4 hours and peaked at 24 hours after retinal ischemia. By the 3rd day after retinal ischemia, the number of cells in GCL was decreased markedly and some cells in GCL and INL were spread out in inner plexiform layer(IPL). Finally, the boundary between GCL and INL became obscure and a few alive cells were found in GCL and INL on 7 days after retinal ischemia. The thickness of the retina was also decreased in a time-dependent manner. IN the study of gene expression in retinal ischemil, p53 expression was increased prominently at 24 hours and 3 days and decreased at 7 days, while Bcl02 expression was increased slightly at 24 hours by RT-PCR and in situ hybridization. ICE expression was not changed in this model. The expression of p53 was also observed at 24 hours after retinal ischemia by immunohistochemistry. With these results it was found that cell death was increased from 4 hours to 3 days after retina ischemia and the thickness of retina decreased markedly during the same period. Delayed neuronal cell death in retina seemed to be correlated with the expression of p53 in the retina ischemia model.
Palabras clave
Texto completo:
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Índice:
WPRIM
Asunto principal:
Retina
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Retinaldehído
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Inmunohistoquímica
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Reperfusión
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Expresión Génica
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Muerte Celular
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Hibridación in Situ
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Neuronas Retinianas
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Hielo
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Presión Intraocular
Límite:
Animals
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Humans
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Male
Idioma:
Ko
Revista:
Journal of the Korean Ophthalmological Society
Año:
1998
Tipo del documento:
Article