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首页> 外文期刊>American Journal of Physiology >Bladder function in mice with inducible smooth muscle-specific deletion of the manganese superoxide dismutase gene
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Bladder function in mice with inducible smooth muscle-specific deletion of the manganese superoxide dismutase gene

机译：膀胱功能在小鼠中，诱导型锰超氧化物歧化酶基因的诱导平滑肌缺失

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摘要

Manganese superoxide dismutase (MnSOD) is considered a critical component of the antioxidant systems that protect against oxidative damage. We are interested in the role of oxidative stress in bladder detrusor smooth muscle (SM) in different disease states. In this study, we generated an inducible, SM-specific Sod2~'~ mouse model to investigate the effects of MnSOD depletion on the function of the bladder. We crossbred floxed Sod2 (Sod2lox/lOK) mice with mice containing heterozygous knock-in of a gene encoding a tamoxifen-activated Cre recombinase in the SM22a promoter locus [SM-CreERT2(ki)Cre/+]. We obtained SoJ2lox/lox,SM-CreERT2(ki)Cre/+ mice and injected 8-wk-old males with 4-hydroxytamoxifen to induce Cre-mediated excision of the floxed Sod2 allele. Twelve weeks later, SM-specific deletion of Sod! and depletion of MnSOD were confirmed by polymerase chain reaction, immunoblotting, and immunohistochemistry. SM-specific Sod2~'~ mice exhibited normal growth with no gross abnormalities. A significant increase in nitrotyrosine concentration was found in bladder SM tissue of SM-specific Sod2~~'~ mice compared with both wild-type mice and Sod2+/+, SM-CreERT2(ki)Cre/+ mice treated with 4-hydroxytamoxifen. Assessment of 24-h micturition in SM-specific Sod2~'~ mice revealed significantly higher voiding frequency compared with both wild-type and SM-specific Cre controls. Conscious cystometry revealed significantly shorter intercontraction intervals and lower functional bladder capacity in SM-specific Sod2~'~ mice compared with wild-type mice. This novel model can be used for exploring the mechanistic role of oxidative stress in organs rich in SM in different pathological conditions.
机译：锰超氧化物歧化酶（MNSOD）被认为是防止氧化损伤的抗氧化系统的关键组分。我们对不同疾病状态的膀胱脱水肌肉（SM）中的氧化压力在膀胱脱水肌中的作用感兴趣。在这项研究中，我们产生了一种诱导的SM特异性SOD2〜'〜鼠标模型，以研究MNSOD耗尽对膀胱功能的影响。我们用含有含有杂合敲入的小鼠在SM22A启动子基因座[SM-Creert2（ki）Cre / +]中含有杂合咔醛的小鼠含有杂合的SOD2（SOD2LOX / LOK）小鼠。我们获得SOJ2LOX / LOX，SM-CREERT2（KI）CRE / +小鼠并注入8-WK型雄性，用4-羟基氧基毒素诱导CRE介导的浮油SOD2等位基因的切除。十二个星期后，SOD的SM特异性删除！通过聚合酶链反应，免疫印迹和免疫组织化学证实了MNSOD的耗尽。 SM特异性SOD2〜'〜小鼠表现出正常的生长，没有总体异常。与用4-羟基氧基毒素处理的野生型小鼠和SOD2 + / +，SM-CREERT2（KI）CRE / +小鼠相比，在SM特异性SOD2〜'〜小鼠的膀胱SM组织中发现硝基酪氨酸浓度的显着增加。与野生型和SM特异性CRE对照相比，SM特异性SOD2〜'〜小鼠中24小时测量术的评估明显较高的空隙频率。有意识的囊谱仪与野生型小鼠相比，SM特异性SOD2〜'〜小鼠中显着较短的间隔和较低的函数膀胱容量。这种新型模型可用于探索在不同病理条件下富含SM的器官氧化应激的机械作用。

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