小鼠中BUBR1功能不足会增加其对氧化应激的敏感性。
BUBR1 Insufficiency in Mice Increases their Sensitivity to Oxidative Stress.
作者信息
Matsuda Daisuke, Matsumoto Takuya, Honma Kenichi, Ikawa-Yoshida Ayae, Onimaru Mitsuho, Furuyama Tadashi, Nakatsu Yoshimichi, Tsuzuki Teruhisa, Maehara Yoshihiko
机构信息
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
出版信息
In Vivo. 2016;30(6):769-776. doi: 10.21873/invivo.10993.
BACKGROUND/AIM: Budding uninhibited by benzimidazole-related 1 (BUBR1) plays an important role in the spindle assembly checkpoint to prevent chromosome missegregation and aneuploidy during mitosis. We previously generated mutant mice that express BUBR1 at only 20% of the normal level (BubR1 mice). Here, we examined the effect of low BUBR1 expression on oxidative stress-induced carcinogenesis in mice.
MATERIALS AND METHODS
We orally administered either a potassium bromate (KBrO) solution (2 g/l) or tap water to BubR1 and wild-type (BubR1)mice for 16 weeks and examined the subsequent incidence of tumours.
RESULTS
KBrO-treated BubR1 mice showed significantly higher mortality than the KBrO-treated BubR1 and control tap water-treated mice (p=0.0082). Histopathological and immunohistochemical analyses revealed that the spleens of surviving BubR1L/L mice were occupied by non-B-, non-T-cells with high proliferative potential.
CONCLUSION
Our results indicate that low BUBR1 expression increases oxidative stress-induced mortality in mice, possibly caused by splenic neoplasms.
背景/目的：苯并咪唑相关1抑制缺陷型芽殖蛋白（BUBR1）在纺锤体组装检查点中发挥重要作用，以防止有丝分裂期间染色体错误分离和非整倍体形成。我们之前培育出了仅表达正常水平20%的BUBR1的突变小鼠（BubR1小鼠）。在此，我们研究了低水平BUBR1表达对小鼠氧化应激诱导的致癌作用的影响。
材料与方法
我们给BubR1小鼠和野生型（BubR1）小鼠口服溴酸钾（KBrO）溶液（2 g/l）或自来水，持续16周，并检查随后的肿瘤发生率。
结果
经KBrO处理的BubR1小鼠的死亡率显著高于经KBrO处理的BubR1小鼠和经对照自来水处理的小鼠（p = 0.0082）。组织病理学和免疫组织化学分析显示，存活的BubR1L/L小鼠的脾脏被具有高增殖潜能的非B、非T细胞占据。
结论
我们的结果表明，低水平BUBR1表达会增加小鼠氧化应激诱导的死亡率，这可能是由脾脏肿瘤引起的。
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