Myocyte apoptosis in the pathogenesis of ureteral damage in rats with obstructive uropathy.
OBJECTIVE
To elucidate the role of signal apoptosis in the pathogenesis of ureteral damage during the course of obstructive uropathy and to investigate the cell proliferation in the smooth muscle layer of ligated ureter.


METHODS
The apoptotic cells were detected with the method of in situ end-labeling of DNA fragments. The expression of Fas, tumor necrosis factor receptor 1 (TNF-R1), and proliferation cell nuclear antigen (PCNA) was examined in 54 rats by immunohistochemistry.


RESULTS
The severity of hydroureter and the histologic changes of ureteral smooth muscle were aggravated during the period of obstruction. The apoptotic cells and the expression of Fas and PCNA in the smooth muscle layer were present since day 14 after ligation. The percentages of apoptotic cells and the expression indexes of Fas and PCNA in the smooth muscle layer progressively increased, reaching a peak on day 21 after ligation, and then declined. The expression of TNF-R1 in the smooth muscle layer was only found on day 21 after ligation. The numbers of the apoptotic cells in the smooth muscle layer correlated significantly with the expression of PCNA, Fas, and TNF-R1. The expression of Fas and TNF-R1 in the smooth muscle layer also correlated significantly. The appearance of apoptotic cells and the expression of Fas and PCNA in the smooth muscle layer were associated with tissue damage and fibrosis in the smooth muscle layer.


CONCLUSIONS
We conclude that cell apoptosis and the expression of Fas, TNF-R1, and PCNA might play important roles in the pathogenesis of ureteral damage in the smooth muscle layer of obstructed ureters.
Chuang
Y
Y
Department of Neurology, Kaohsiung Medical University School of Medicine, Republic of China, Kaohsiung, Taiwan.
Chuang
W
W
Huang
C
C
D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology*; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D006869:Hydronephrosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D006984:Hypertrophy; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008026:Ligation; D009000:Monocytes / Q000378:metabolism / Q000502:physiology*; D009130:Muscle, Smooth / Q000378:metabolism / Q000503:physiopathology*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D047888:Receptors, Tumor Necrosis Factor, Type I; D014513:Ureter / Q000378:metabolism / Q000503:physiopathology*; D014517:Ureteral Obstruction / Q000378:metabolism / Q000503:physiopathology*; D019014:fas Receptor / Q000378:metabolism
D015703:Antigens, CD; D018809:Proliferating Cell Nuclear Antigen; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D019014:fas Receptor