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机构地区:[1]长江大学医学院组织学与胚胎学系,荆州434000 [2]北京大学基础医学院解剖学与组织学胚胎学系,北京100091
出 处:《解剖学杂志》2010年第1期26-28,共3页Chinese Journal of Anatomy
摘 要:目的:观察Smad3基因敲除小鼠肾Smad2和p-Smad2表达的变化,探讨Smad3基因敲除小鼠肾是否有Smad2和p-Smad2代偿性增加。方法:4只Smad3基因敲除小鼠,10只野生型小鼠,应用免疫组织化学显色技术,检测Smad2和矿Smad2蛋白的定位和表达情况,并用Modc病理图像分析系统对图像进行半定量分析。结果:野生型小鼠肾Smad2蛋白在肾远端小管和肾集合管细胞胞质中有广泛弱表达,p-Smad2蛋白在肾远端小管和肾集合管细胞胞质、胞核中也有弱表达,而Smad3基因敲除小鼠的Smad2和p-Smad2的表达比野生型小鼠有显著升高。结论:Smad3基因敲除能引起小鼠肾Smad2和p-Smad2表达的代偿性增加。Objective: To study the changes of Smad2/p-Smad2 expression in the kidney of Smad3 knock-out mice. Methods: The expressions and localization of Smad2 and p-Smad2 proteins in the kidney of wide-type and Smad3 knockkout mice were examined by immunohistochemistry. Results: Smad2 protein was widely and weakly expressed in cytoplasm in distal renal tubules and collecting ducts of the wide-type mice, and p Smad2 protein was mainly expressed in the nuclei of collecting duets and distal tubules. The expression of Smad2 and p-Smad2 protein was significantly increased in the Smad3 knockout mice (P 〈 0.01). Conclusion: Smad3 knock-out can cause a compensatory increase in the expression of Smad2 and p-Smad2 protein in the kidney of mice.
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