Renal cell turnover results in a fine balance between apoptosis and cell proliferation
JUANJOSÉ BOLLAIN-Y-GOYTIA1, ESTEBAN MEZA-LAMAS1, ADRIAÚN LOÚPEZ1, ESPERANZA AVALOS-DIÚAZ1, CRISTINA RODRIÚGUEZ-PADILLA2 and RAFAEL HERRERA-ESPARZA1*

1 Department of Molecular Biology, Institute for Experimental Biology, Universidad AutoÚnoma de Zacatecas, Guadalupe, Zacatecas, México
2 Department of Immunology, School of Biological Sciences, Universidad AutoÚnoma de Nuevo LeoÚn, Monterrey, Nuevo LeoÚn, México


Abstract

Renal cell turnover (RCT) results in a fine balance between apoptosis and cell proliferation. RCT starts early in developing mammalian kidneys and after birth it supports the structure and function of the kidney. After renal inflammation, the role of RTC is critical in repair. Current studies have been addressed to whether apoptosis participates in renal cell turnover at different stages of renal life. Kidneys were obtained from a group of newborn and adult normal Balb/c mice. Tissues were preserved in RNAlater, and sections were obtained and processed with the TUNEL method. The protein expression of fas, fasL and pcna was studied by immunofluorescence. The expression of the fas, fasL, caspase 3, dff40, pcna and g3pdh genes was determined by RT-PCR. Results showed a low apoptotic rate in kidneys of newborn mice. However, this rate progressively increased by elderly. On the opposite, a high cell proliferation and transcription of pcna was observed in newborn mice which declined by elderly. Our study demonstrated that apoptosis is a normal process in the kidney. Apoptosis is increased by elderly and is concurrent with a decline of cell proliferation. Both mechanisms contribute to maintain renal cell turnover. This work attempts to provide a rational of the renal development which can be applied for better comprehension of the molecular mechanisms on renal pathology and novel designs of therapeutic interventions.


 
< back
.