Characterization of the testis in congenitally ubiquitin carboxy-terminal hydrolase-1 (Uch-L1) defective (gad) mice

被引:43
作者
Kwon, J
Kikuchi, T
Setsuie, R
Ishii, Y
Kyuwa, S
Yoshikawa, Y
机构
[1] Univ Tokyo, Grad Sch Agr & Life Sci, Dept Biomed Sci, Bunkyo Ku, Tokyo 1138657, Japan
[2] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Anim Models Human Dis, Tokyo 1878502, Japan
关键词
gad mice; seminiferous tubules; proliferating cell nuclear antigen (PCNA); testis; ubiquitin carboxy-terminal hydrolase-1 (Uch-L1);
D O I
10.1538/expanim.52.1
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
The gracile axonal dystrophy (gad) mice are known to have a deletion within the gene encoding ubiquitin carboxy-terminal hydrolase-1 (Uch-L1) and show hereditary sensory deterioration and motor paresis. Expression of Uch-L1 is reported to be almost limited to the nervous system and testis. To understand whether Uch-L1, one of the major ubiquitin carboxy-terminal hydrolase (UCH) isozymes in the testis, affects spermatogenesis and other UCH isozymes (Uch-L3, L4 and L5) expression in the testis, we compared the testis between gad, hetero and wild type mice by histological, immunohistochemical analyses and RT-PCR. Histological analysis in 25-week-old gad mice showed shrinking of seminiferous tubules, decreasing total number of cells and enlargement of remaining cells in seminiferous tubules. By immunohistochemistry, a significant decrease (p<0.05) in the number of proliferating cell nuclear antigen (PCNA) positive cells was observed. Expression of other UCH isozyme mRNAs was not apparently affected by Uch-L1 deficiency in 25-week-old gad mice. This study is the first report on the testis of gad mutant mouse.
引用
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页码:1 / 9
页数:9
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