背景:Sema7A是一种细胞表面蛋白,它可以促进破骨细胞的融合同时促进成骨细胞的迁移,从而影响骨的动态平衡。推测,Sema7A siR NA可能减弱钛微粒成骨细胞分化。目的:分析信号素7A(Sema7A)对钛颗粒抑制鼠MC3T3-E1前成骨细胞活性过程的影响...
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背景:Sema7A是一种细胞表面蛋白,它可以促进破骨细胞的融合同时促进成骨细胞的迁移,从而影响骨的动态平衡。推测,Sema7A siR NA可能减弱钛微粒成骨细胞分化。目的:分析信号素7A(Sema7A)对钛颗粒抑制鼠MC3T3-E1前成骨细胞活性过程的影响。方法:取第六七代生长状态良好的小鼠颅骨前成骨细胞(MC3T3-E1),分为4组培养。其中空白对照组为单独培养的细胞;标准对照组加入了钛微粒共培养;实验1组加入Sema7A过表达质粒,实验2组加入Sema7AsiR NA进行干扰。采用流式细胞仪检测细胞凋亡情况;Q-PCR检测骨涎蛋白、骨钙素、Ⅰ型胶原蛋白的mR NA表达情况;Western-blot检测骨涎蛋白、骨钙素、Ⅰ型胶原蛋白的蛋白表达情况;茜素红钙结节染色检测成骨细胞的矿化程度。结果与结论:结果提示标准对照组、实验1组检测到骨涎蛋白、骨钙素、Ⅰ型胶原蛋白表达明显减少而实验2组骨涎蛋白、骨钙素、Ⅰ型胶原蛋白则比标准对照组表达增加(P<0.05)。流式细胞仪结果提示实验1组成骨细胞凋亡率明显高于其他组(P<0.05),而实验2组则比标准对照组凋亡率降低(P<0.05)。茜素红染色检测结果显示实验1组未见明显的矿化结节,实验2组有矿化结节形成。结果表明通过基因干扰技术抑制Sema7A活性可以对钛颗粒抑制鼠MC3T3-E1成骨细胞分化的过程进行干扰,进而为临床上用生物技术治疗磨损微粒诱导的骨溶解问题提供了一条可行的思路。
The discovery of Sema 4D can be dated to 1992,when Boumsell's team reported a novel 150-kDa glycoprotein *** was expressed on T lymphocytes that had been activated with CD3 monoclonal antibody or phytohaemagglufin...
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The discovery of Sema 4D can be dated to 1992,when Boumsell's team reported a novel 150-kDa glycoprotein *** was expressed on T lymphocytes that had been activated with CD3 monoclonal antibody or phytohaemagglufinin.1Hence,this molecule has been designated CD100 by the Intemational Workshop on Human Leukocyte Differentiation *** 1996,3 years after the discovery of the semaphorin family,2 the CD100 gene was cloned and identified as the first semaphorin with immune system functions.3Unlike the prototypical semaphorins,which are neuronal chemorepellents,Sema 4D/CD100 together with Sema 3A,Sema 4A,Sema 6D and Sema 7A have been described as 'immune semaphorins',because they are expressed on T cells,B cells,natural killer cells and dendritic cells,and exhibit a variety of immunological functions.
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