Objective Apolipoprotein E （apoE） is associated with increased risk of age-related diseases, such as Alzheimer＇s disease （AD） and cerebrovascular disease （CVD）. The present study aims to investigate the age-rel...
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Objective Apolipoprotein E （apoE） is associated with increased risk of age-related diseases, such as Alzheimer＇s disease （AD） and cerebrovascular disease （CVD）. The present study aims to investigate the age-related general morphological changes of the brain in GFAP-apoE transgenic mice, especially the alterations in number and size of hippocampal pyramidal cells and the microvascular lesions in the thalamus. Methods Nine female apoE4/4 mice were divided into 3 groups （n=3 in each group）： 3-4 months （young group）, 9-10 months （middle-aged group） and 20-21 months （old group）. Age-matched apoE3/ 3 mice were employed as control group （n=3 in each group）. The paraffin sections of brain tissue were stained by 2 conventional staining methods, thionin staining and hematoxylin-esion（HE） staining, the former of which was to observe the hippocampal cells, while the latter was used to examine the brain microvasculature. Results There was no apparent difference in the cortical layer between apoE3/3 and apoE4/4 mice, neither any significant difference in the number of cells in hippocampal CA1-CA3 subfields between apoE3/3 and apoE4/4 mice at various age points （P 〉 0.05）. However, the mean size of pyramidal cells in CA1 subfield in apoE3/3 and apoE4/4 mice decreased as mice were getting older （P 〈 0.001）. At the age of 20-21 months, this cellular atrophy in apoE4/4 mice was more severe than that in old apoE3/3 mice （P 〈 0.05）. Furthermore, microvascular lesion in the thalamus was detected in all the 3 old apoE4/4 mice, at varying degrees （5.24%, 1.41% and 3.97%, respectively）, while only one apoE3/3 mouse exhibited microvascular lesion in the thalamus, at a low level （0.85%）. Conclusion The current study suggests that the cell size in hippocampal CA1 subfield decreases with aging, irrespective of apoE genotype. Cellular atrophy in CA1 subfield and the microvascular lesion in the thalamus are both more severe in old apoE4/4 mice as compared with those in age-matched apoE3/3 mice.
纺锤体检验点(spindle checkpoint)是一个重要的细胞分裂生化调节通路,可监督染色体正确分离和传代.着丝粒相关蛋白E(centromere-associated protein E,CENP-E)是一个分子量为312kD的微管马达驱动蛋白,可以衔接纺锤体微管与动点并参与...
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纺锤体检验点(spindle checkpoint)是一个重要的细胞分裂生化调节通路,可监督染色体正确分离和传代.着丝粒相关蛋白E(centromere-associated protein E,CENP-E)是一个分子量为312kD的微管马达驱动蛋白,可以衔接纺锤体微管与动点并参与纺锤体检验点调控.为研究CENP-E的作用机理,以其动点结合区域为诱饵蛋白,用酵母双杂交技术从人HeLa细胞cDNA文库中筛选出了Nuf2蛋白.体外的pull-down实验和体内的免疫共沉淀实验表明,Nuf2蛋白通过其卷曲螺旋(coiled-coil)功能域特异结合CENP-E的C末端区域,间接免疫荧光显示Nuf2与CENP-E共定位于细胞有丝分裂期染色体的动点.由此推论,CENP-E通过Nuf2的直接作用参与构筑动点-微管界面,进而参与细胞有丝分裂纺锤体检验点信号转导通路,为染色体正确分离发挥调控作用.
目的观察Bcl-2和Bax高脂饮食大鼠肾组织中Bcl-2和Bax表达及细胞凋亡,探讨脂质肾毒性损伤的机制。方法将10只雄性SD大鼠随机均分为对照组和高脂饮食组,喂养6周,检测血清学指标;用HE染色观察肾脏组织学改变;采用TUNEL法检测细胞凋亡情况;免疫组化方法检测Bcl-2和Bax表达。结果高脂饮食组血清甘油三酯(TG)、总胆固醇(TC)水平明显高于对照组,而高密度脂蛋白胆固醇(HDL-C)水平明显下降(P<0.05);高脂饮食组肾组织凋亡细胞数高于对照组(高倍镜视野15.45±5.07 vs 3.57±1.38,P<0.05),且肾小管的凋亡细胞明显多于肾小球;高脂饮食组Bax平均光密度高于对照组(0.2763±0.0912 vs 0.1506±0.3334,P<0.05),Bcl-2平均光密度低于对照组(0.2450±0.0216 vs 0.2941±0.0204,P<0.05)。结论高脂饮食可导致大鼠肾组织中凋亡细胞增多,且Bcl-2、Bax的表达及Bcl-2/Bax影响着肾脏组织细胞凋亡的发生。
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