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作 者:孙彧[1] 张丽娉[1] 陈仁华[1] 邹云增[2] 李毅刚[1]
机构地区:[1]上海交通大学医学院附属新华医院心内科,200092 [2]上海复旦大学附属中山医院心内科,200032
出 处:《国际心血管病杂志》2011年第5期301-304,共4页International Journal of Cardiovascular Disease
基 金:国家自然科学基金(30871082);国家自然科学基金(81070154);上海市科学技术委员会科研计划项目(10XD1402800)
摘 要:目的:研究缺氧大鼠乳鼠心肌细胞中信号素3A(sema3a)与p-connexin 43(Ser 279/282)的相关性变化。方法:体外培养大鼠乳鼠心肌细胞并缺氧,检测sema3a与p-connexin 43(Ser 279/282)在不同缺氧时间的变化。慢病毒构建并转染心肌细胞,分为空白组、空病毒组、病毒组3组,选择在最佳缺氧时间点检测sema3a及p-connexin43(Ser 279/282)的蛋白水平变化。结果:(1)1 h为检测最佳缺氧时间点,p-connexin43(Ser 279/282)在1 h缺氧组达到高峰(P<0.05),sema3a缺氧12 h急剧下降(P<0.05)。(2)高表达sema3a,p-connexin 43(Ser 279/282)降低;抑制表达sema3a,p-con-nexin 43(Ser 279/282)升高。结论:在缺氧条件下,sema3a可以负向调节p-connexin43(Ser 279/282),影响缝隙连接功能,提示其在影响细胞间电传导、诱发室性心律失常中有重要作用。Objective:To investigate the correlation of sema3a and p-connexin 43 (Set 279/282) in cultured neonatal rat ventricular myoeytes during hypoxia. Methods:Cultured neonatal rat ventricular myocytes were exposed to hypoxia (1% 02 ),sema3a and p-connexin 43 (Ser 279/282) expressions were analyzed at different hypoxie time. Then cultured ventricular myoeytes were transfected with lentivirus to overexpress or downregulate sema3a, p-connexin 43 (Ser 279/282) level was measured under hypoxia, in control, GFP-lentivirus, sema3a overexpression and si-ema3a group, respectively. Resuits.. (1) P-connexin 43 (Ser 279/282) increased to the peak at lh hypoxia(P〈0.05),sema3a sharply decreased at 12h hypoxia(P〈0.05). (2) P-connexin 43 (Ser 279/282) decreased following sema3a upregulation; p-connexin 43 (Ser 279/282) increased following sema3a downregualtion. Conclusion:Under hypoxic conditions, sema3a can negatively regulate p-connexin 43 (Ser 279/282) level disrupt gap junctional communication. It indicates that sema3a plays an important role in affecting intercellular electrical conduction and contribute to the generation of the ventricular arrhythmogenic substrate.
关 键 词:信号素3A 连接蛋白43 缝隙连接 室性心律失常
分 类 号:R541.7[医药卫生—心血管疾病]
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