Characterization of the testis in congenitally ubiquitin carboxy-terminal hydrolase-1 (Uch-L1) defective (gad) mice
Characterization of the testis in congenitally ubiquitin carboxy-terminal hydrolase-1 (Uch-L1) defective (gad) mice
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DOI：
10.1538/expanim.52.1
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发表时间：
2003-01-01
影响因子：
2.4
通讯作者：
Yoshikawa, Y
中科院分区：
文献类型：
--
作者：
Kwon, J;Kikuchi, T;Yoshikawa, Y
已知纤细轴突营养不良（gad）小鼠在编码泛素羧基末端水解酶-1（Uch-L1）的基因内具有缺失，并且显示遗传性感觉退化和运动性轻瘫。据报道，Uch-L1的表达几乎仅限于神经系统和睾丸。为了了解Uch-L1，在睾丸中的主要泛素羧基末端水解酶（UCH）同工酶之一，是否影响精子发生和其他UCH同工酶（Uch-L3，L4和L5）在睾丸中的表达，我们比较了gad，异源和野生型小鼠的睾丸组织学，免疫组织化学分析和RT-PCR。25周龄gad小鼠的组织学分析显示曲细精管萎缩，曲细精管中细胞总数减少，剩余细胞增大。免疫组化显示，
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