Transcription profiling of mouse aorta genes of APOE-deficient animals receiving the ACE inhibitor captopril

Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages. Experiment Overall Design: Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to captopril-treated APOE-deficient mice, and nontransgenic control mice. Three study groups were analyzed, i.e. 8-months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the angiotensin-converting enzyme (ACE) inhibitor, captopril (20 mg/kg in drinking water), and nontransgenic control C57BL/6J mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip.载脂蛋白E（APOE）缺陷小鼠接受血管紧张素转换酶（ACE）抑制剂卡托普利进行动脉粥样硬化治疗后的主动脉基因芯片表达谱分析。 高胆固醇血症载脂蛋白E缺陷小鼠作为动脉粥样硬化标准模型，用于研究卡托普利介导的动脉粥样硬化治疗过程中的基因表达变化。 本研究对分离自卡托普利处理的APOE缺陷小鼠、未接受治疗且已出现显性动脉粥样硬化的APOE缺陷小鼠，以及非转基因对照小鼠的完整主动脉开展了基因芯片分析。 基因芯片表达谱分析结果显示，卡托普利介导的动脉粥样硬化预防作用，涉及对主动脉浸润的致动脉粥样硬化性免疫细胞（如促动脉粥样硬化T淋巴细胞与巨噬细胞）的抑制。 实验总体设计：本研究对分离自动脉粥样硬化APOE缺陷小鼠、卡托普利处理的APOE缺陷小鼠，以及非转基因对照小鼠的完整主动脉开展基因芯片表达谱分析。 本研究共设置3个实验组别：分别为8月龄、已出现显性动脉粥样硬化的未处理APOE缺陷小鼠；年龄匹配、经血管紧张素转换酶（ACE）抑制剂卡托普利（饮用水中给药浓度为20mg/kg）持续处理7个月的APOE缺陷小鼠；以及非转基因对照C57BL/6J小鼠。 每组均设置2次生物学重复，每1份基因芯片样本混合3份主动脉的总RNA。