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目的:初步探讨microRNA-155(miR-155)在慢性心房颤动(房颤)中3型小电导钙激活钾通道(SK3)重构中的作用.方法:将67例心脏瓣膜病外科手术患者分为房颤组(31例)和窦律组(36例),利用实时荧光定量PCR分别检测两组患者右心耳miR-155与SK3 mRNA表达水平,免疫印迹法检测SK3蛋白表达水平;分别利用miR-155 mimic和miR-155 inhibitor干预人心肌细胞系(AC16细胞系),观察其对AC16细胞SK3 mRNA和蛋白表达水平的影响.结果:房颤组右心耳miR-155表达水平较窦律组显著上调(1.292±0.261∶0.310土0.161,P＜0.01).房颤组右心耳SK3 mRNA表达水平与窦律组无显著差异(0.855±0.295∶0.917±0.253,P＞0.05),但房颤组右心耳SK3蛋白表达水平较窦律组显著下调(0.182±0.043∶0.302±0.064,P＜0.01).两组患者右心耳miR-155表达水平与SK3蛋白表达水平呈负相关(r=-0.735,P＜0.01).miR-155 mimic减少AC16细胞SK3蛋白表达,而miR-155 inhibitor则增加SK3蛋白表达,但两者均对SK3 mRNA的表达无影响.结论:慢性房颤患者右心房miR-155表达上调,可能通过下调SK3表达水平,参与房颤的发生与维持.“,”Objective:To investigate the effect of microRNA-155 (miR-155) on remodeling of small conductance calcium activated potassium channel 3 (SK3) in human chronic atrial fibrillation (AF).Method:Right atrial appendages were obtained from 67 patients undergoing cardiac surgery,including 31 patients with chronic AF and 36 patients with sinus rhythem (SR).The expression level of miR-155 was determined by real-time quantitative PCR.The mRNA or protein levels of SK3 were determined by real-time quantitative PCR Western blot,respectively.miR-155 mimic and miR-155 inhibitor were transfected into AC16 cells,respectively.Result:The expression of miR-155 was found to be significantly up-regulated in AF patients compared with patients with SR (1.292 ± 0.261 vs 0.310±0.161,P＜0.01).No significant difference at the mRNA expression level of SK3 was found between patients with AF and patients with SR (0.855±0.295 vs 0.917±0.253,P＞0.05),but the protein expression of SK3 in patients with AF was significantly lower than that of patients with SR (0.182±0.043 vs 0.302 ±0.064,P＜0.01).There was a negative correlation between the expression level of miR-155 and the protein expression level of SK3 in right atrial appendage (r=-0.735,P＜0.01).miR-155 mimic reduced the protein expression of SK3 in AC16 cells,while miR-155 inhibitor increased the protein expression of SK3,but both had no effect on the mRNA expression of SK3.Conclusion:Upregulation of miR-155 may contribute to atrial electrical remodeling in human atrial fibrillation by targeting SK3.