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作 者:王吉静[1] 李玉琳[1] 王月丽[1] 郑帅[1] 贾立昕[1] 王绿娅[1] 杜杰[1]
机构地区:[1]首都医科大学附属北京安贞医院心血管重塑相关疾病教育部重点实验室,北京市100029
出 处:《中国分子心脏病学杂志》2014年第1期830-833,共4页Molecular Cardiology of China
基 金:国家自然基金(NO:81230006;31090363)
摘 要:目的研究高血压早期血管损伤中基因表达变化。方法 30只8周龄雄性C57BL/6J小鼠随机分为对照组和血管紧张素II(angiotensin II,Ang II)组,采用植入式胶囊渗透压泵分别灌注生理盐水和Ang II 1500 ng/(kg·min),于第7天取主动脉,提取RNA后进行基因芯片分析;采用鼠尾套法检测小鼠尾动脉血压、超声检测心脏结构及功能;实时定量PCR(Real-time PCR)检测骨桥蛋白(OPN)的表达;取其胸主动脉进行组织切片,免疫组织化学染色观察骨桥蛋白的表达。结果与对照组相比,Ang II组在灌泵7天时血压升高[(105±7)vs.(148±14)mmHg,1mm Hg=0.133 kPa,P<0.001];基因芯片结果显示骨桥蛋白基因表达明显升高(>50倍);real-time PCR验证骨桥蛋白表达升高3.9±0.9倍,P<0.05;免疫组化显示主动脉OPN表达增加。结论 Ang II导致高血压情况下,血管组织OPN表达增高,可能参与高血压血管损伤的过程。Objective To identify the genes of which responsible for hypertension induced vascular injury. Methods 30 C57BL/6J male mice were randomly divided into control group (n=15) and angiotensin II group (n=15), using osmotic mini-pumps were implanted capsules infusion saline and Ang II 1500 ng/(kg, min); Blood pressure and cardiac function were measured by tail-cuff plethysmography method and evaluated by ultrasonography. At day 7, Ang II- or saline- treated mice were euthanized, and the mRNAs were isolated from thoracic aorta of control and treated mice and were analyzed by microarray. The thoracic aorta were analyzed for real-time PCR and immunohistochemistry. Results Compared with the control group, blood pressure was significantly increased at 7 days after Ang II infusion [(105±7 vs. (148+14) mmHg, P〈0.001]; microarray analysis showed that osteopontin (OPN) was significantly unregulated in Ang II infused thoracic aorta (〉50-fold); Both real-time PCR and immunohistochemistry confirmed that OPN expression in aorta from Ang II-infused animals was significantly increased (P〈0.05); Conclusion Ang II infusion leads to hypertension and increases OPN expression, given the facts of multifunctional OPN, elevated OPN could be responsible for hypertension-induced vascular injury.
关 键 词:高血压 血管损伤 炎症反应 骨桥蛋白 血管紧张素II
分 类 号:R544.1[医药卫生—心血管疾病]
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