解剖学杂志
解剖學雜誌
해부학잡지
CHINESE JOURNAL OF ANATOMY
2010年
1期
26-28
,共3页
Smad2%p-Smad2%Smad3基因敲除%小鼠
Smad2%p-Smad2%Smad3基因敲除%小鼠
Smad2%p-Smad2%Smad3기인고제%소서
Smad2%p-Smad2%Smad3 knock-out%mouse
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p-Smad2蛋白的定位和表达情况,并用Motic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.
目的:觀察Smad3基因敲除小鼠腎Smad2和p-Smad2錶達的變化,探討Smad3基因敲除小鼠腎是否有Smad2和p-Smad2代償性增加.方法:4隻Smad3基因敲除小鼠,10隻野生型小鼠,應用免疫組織化學顯色技術,檢測Smad2和p-Smad2蛋白的定位和錶達情況,併用Motic病理圖像分析繫統對圖像進行半定量分析.結果:野生型小鼠腎Smad2蛋白在腎遠耑小管和腎集閤管細胞胞質中有廣汎弱錶達,p-Smad2蛋白在腎遠耑小管和腎集閤管細胞胞質、胞覈中也有弱錶達,而Smad3基因敲除小鼠的Smad2和p-Smad2的錶達比野生型小鼠有顯著升高.結論:Smad3基因敲除能引起小鼠腎Smad2和p-Smad2錶達的代償性增加.
목적:관찰Smad3기인고제소서신Smad2화p-Smad2표체적변화,탐토Smad3기인고제소서신시부유Smad2화p-Smad2대상성증가.방법:4지Smad3기인고제소서,10지야생형소서,응용면역조직화학현색기술,검측Smad2화p-Smad2단백적정위화표체정황,병용Motic병리도상분석계통대도상진행반정량분석.결과:야생형소서신Smad2단백재신원단소관화신집합관세포포질중유엄범약표체,p-Smad2단백재신원단소관화신집합관세포포질、포핵중야유약표체,이Smad3기인고제소서적Smad2화p-Smad2적표체비야생형소서유현저승고.결론:Smad3기인고제능인기소서신Smad2화p-Smad2표체적대상성증가.
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 knock-out 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 ducts and distal tubules. The expression of Smad2 and p-Smad2 protein was significantly increased in the Smad3 knock-out 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.