The Expressions of p53, gamma-H(2)AX and Ku70/Ku80 That was Caused by Hydronephrosis in the Kidney of Rats / 대한비뇨기과학회지
Korean Journal of Urology
;
: 976-983, 2007.
Artículo
en Coreano
| WPRIM
| ID: wpr-78520
ABSTRACT
PURPOSE:
There are little research about the factors of DNA damage and repair that might cause renal parenchymal damage under the condition of hydronephrosis. In this study, we studied the expressions of p53, gamma-H(2)AX and Ku70/Ku80 in rat kidney under the condition of hydronephrosis. MATERIALS ANDMETHODS:
16 Sprague-Dawley rats that were 7~8 weeks old were used. Partial ureteral obstruction was induced in 12 rats. And for the other 4 rats, a sham-operation was done as a control. The hydronephrosis-induced rats had their right kidney removed after 1, 2 and 3 weeks and the sham-operated rats underwent nephrectomy after 3 weeks. Those removed tissues were examined with immunohistochemical staining and western blot to confirm the degree of expression of p53, gamma-H(2)AX and Ku70/Ku80.RESULTS:
The expressions of p53, gamma-H(2)AX and Ku70/Ku80 caused by hydronephrosis in the rat increased as time passed, and these expressions of controls were in a low level or they were negative. These results were similar with the results of the immunohistochemical staining and Western blot.CONCLUSIONS:
This study confirmed that the protein expressions of gamma- H(2)AX, p53, and Ku70/Ku80 are increased, and these expressions are the DNA damage-related factors in the renal parenchyma of hydronephrosis-induced rats. We confirmed the possibility that DNA double strand breaks (DSBs) might be the main mechanism that induces renal parenchymal damage under the condition of hydronephrosis.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Obstrucción Ureteral
/
Daño del ADN
/
ADN
/
Western Blotting
/
Ratas Sprague-Dawley
/
Reparación del ADN
/
Roturas del ADN de Doble Cadena
/
Hidronefrosis
/
Riñón
/
Nefrectomía
Límite:
Animales
Idioma:
Coreano
Revista:
Korean Journal of Urology
Año:
2007
Tipo del documento:
Artículo
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