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.
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