Sequential Renal Changes in Uninephrectomized Rabbits at Different Stage of Growth : Study on Morphometric Analysis, Cell Proliferation and Apoptosis.
- Author:
Seok Hoon JEON
1
;
Jung Woo NOH
;
Moon Hyang PARK
Author Information
1. Department of Pathology, College of Medicine, Hanyang University, Korea. parkmh@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Kidney;
Uninephrectomy;
Hypertrophy;
Apoptosis;
Ki-67;
Rabbits
- MeSH:
Apoptosis*;
Cell Proliferation*;
Humans;
Hypertrophy;
In Situ Nick-End Labeling;
Ki-67 Antigen;
Kidney;
Male;
Rabbits*;
Weights and Measures
- From:Korean Journal of Nephrology
2002;21(4):531-545
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: After uninephrectomy(UNX), proliferation and apoptosis of renal cells are regarded to be closely involved in glomerular hypertrophy and compensatory renal growth. However, exact mechanism has not been well elucidated in relation with the growing status. METHODS: In small, medium and large male New Zealand white rabbits, unilateral kidneys obtained 1, 7, and 30 days after Sham operation were used for control. In experimental groups, the rabbits were sacrificed, and residual kidneys were obtained 1, 7, and 30 days after UNX. Morphometric analysis of glomerular size were performed. Immunohistochemical staining for MIB-1 antigen and Tdt-mediated dUTP-digoxigenin nick end labelling(TUNEL) method were performed. RESULTS: Glomerular hypertrophy was demonstrated in all groups after UNX and pronounced in the small rabbits. The number of renal Ki-67 positive cells were progressively increased in all study groups. The number of TUNEL positive cells was relatively small in controls. however, the numbers of glomerular, tubular and interstitial TUNEL positive cells were progressively increased in all study groups. CONCLUSION: These results demonstrate that different results regarding the compensatory growth in uninephrectomized rabbits of different weights and ages. Apoptosis may play an important role in the regression of hypertrophic and proliferated glomerular and tubulointerstitial cells during compensatory renal hypertrophy.
