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目的:探讨微小RNA(microRNA，miR)-155对人胚胎干细胞(hESCs)诱导分化的心房肌细胞L-型钙通道α1c(Cav1.2)钙电流(In Ca-L)、基因及蛋白表达的影响。n 方法:诱导并鉴定H7hESCs(购自中国科学院)分化获得的人心房肌细胞(分化第8～10天可获得)，向心肌细胞转染含有miR-155前体序列或反义序列的慢病毒，分为对照组、miR-155模拟物(Mimics)组、miR-155抑制子(Inhibitors)组。于72 h后，运用膜片钳、实时定量反转录聚合酶链反应(RT-qPCR)以及蛋白质印迹法(Western blot)检测In Ca-L、mRNA及蛋白的变化。组间比较采用n t检验，多组间比较采用单因素方差分析。n 结果:成功获得心房肌细胞，转染miR-155模拟物后，miR-155表达高于对照组(25.52±3.63比1.00±0.00，n t＝11.713，n P<0.05)，差异有统计学意义。转染miR-155抑制子后，miR-155表达低于对照组(0.59±0.07比1.00±0.00，n t＝10.933，n P<0.05)，差异有统计学意义。膜片钳结果发现miR-155上调组In Ca-L明显低于对照组(-9.79±3.70比-14.27±3.95，n t＝2.611，n P<0.05)，差异有统计学意义，RT-qPCR及Western blot证实，miR-155上调组Cav1.2的mRNA表达量(0.45±0.06比1.00±0.00，n t＝17.226，n P<0.05)及蛋白表达量(0.71±0.07比1.00±0.00，n t＝7.708，n P<0.05)均低于对照组，差异均有统计学意义。n 结论:对于hESCs诱导的心房肌细胞，上调miR-155可导致Cav1.2蛋白表达水平下降，In Ca-L电流减小，可能参与心房肌细胞的电重构。n “,”Objective:To investigate the effects of microRNA (miRNA, miR)-155 on L-type calcium channel α1c (Cav1.2) of atrial myocytes induced by human embryonic stem cells (H7 line) in calcium current L-type calcium channel current(I n Ca-L) and related gene and protein expression.n Methods:The human embryonic stem cell (hESCs) were induced to differentiate into atrial myocytes (on the day 8-10), which were then infected by lentivirus (including pre-miR-155 or anti-miR-155). The atrial myoctes were divided into control group, miR-155 mimic group and miR-155 inhibitor group. At 72 h, changes in In Ca-L were measured by patch clamp and corresponding mRNAs by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR). The expression of Cav1.2 was detected by Western blotting. Analysis was performed using statistic package for social science (SPSS) 20.0 software. Student′s n t test was used to compare the two sample means. And one-way anova was used for comparison of results between multiple groups.n Results:Atrial myocytes were obtained, and after transfection with miR-155 mimics, the expression of miR-155 was significantly up-regulated (25.52±3.63 vs. 1.00±0.00, n t=11.713, n P<0.05) as compared with control group. After transfection with mir-155 inhibitors, the expression of miR-155 was significantly down-regulated (0.59±0.07 vs. 1.00±0.00,n t=10.933, n P<0.05). The result of patch clamp showed that In Ca-L decreased (-9.79±3.70 vs. -14.27±3.95, n t=2.611, n P<0.05) in miR-155 up-regulation group. Meanwhile, it was verified that the mRNA (0.45±0.06 vs. 1.00±0.00,n t=17.226, n P<0.05) and protein (0.71±0.07 vs. 1.00±0.00,n t=7.708, n P<0.05) of Cav1.2 were both obviously reduced in miR-155 up-regulation group by RT-qPCR and Western blotting.n Conclusion:The up-regulation of miR-155 in atrial myocytes from hESCs could repress the protein expression of Cav1.2, leading to the reduction of In Ca-L, which may became one molecular basis of atrial electrical remodeling.n