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心房颤动患者心房组织延迟整流钾通道基因表达的研究 被引量:9

Gene expression of atrial delayed rectifier potassium channels in human atrial fibrillation
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摘要 目的探讨心房颤动(AF)患者心房组织延迟整流钾通道(Kv1.5、HERG、KvLQT1通道) 基因表达的变化。方法以窦性心律组(SR组)为对照,应用逆转录-聚合酶链反应(RT-PCR),以三磷酸甘油醛脱氢酶(GAPDH)为内参照,检测35例风湿性心脏瓣膜病患者右心耳组织Kv1.5、HERG、Kv- LQT1通道的mRNA表达量。结果和SR组相比,Kv1.5钾通道mRNA表达在慢性房颤组(CAF组)下降显著,有统计学意义(P<0.05),在阵发性房颤组(PAF组)差异无统计学意义(P>0.05);HERG钾通道和KvLQT1钾通道mRNA表达CAF组和PAF组差异均无统计学意义(P>0.05)。结论Kvl.5钾通道转录水平下调可能是相应超速延迟整流钾电流(Ikur)重构的分子基础,其基因表达异常是AF电重构的重要环节;HERG钾通道和KvLQT1钾通道在基因转录水平差异无统计学意义,与AF模型快速延迟整流钾电流(Ikr)和缓慢延迟整流钾电流(Iks)无变化相符。 Objective To investigate the gene expression of delayed rectifier potassium channels (Kv1. 5 ,HERG and KvLQT1 potassium channel ) in human atrial fibrillation (AF). Methods The mRNA amount of Kv1. 5, HERG and KvLQT1 genes was measured by reverse transcription-polymerse chain reaction (RT-PCR) and normalized to the mRNA content of glyceraldehydes-3phosphate dehydrogenase (GAPDH) in 35 patients with rheumatic heart disease. Subjects with sinus rhythm ( SR ) were considered as control group. Results The mRNA content of Kvl. 5 was decreased significantly in patients with CAF ( P 〈 0. 05 ) and remained stable in patients with PAF(P 〉0. 05 ) ,compared with that in patients with SR , there were no significant changes in mRNA content of HERG and KvLQT1 in all groups ( P 〉 0. 05 ). Conclusion The down-regulation of the gene expression of atrial Kv1. 5 may serve as the molecular basis of ultra rapid delayed rectifier current ( IKur ) remodeling in patients with CAF. The mRNA expression of HERG and KvLQT1, keep stable in patient with AF, which accords with the eletrophysiological study of fast delayed rectifier potassium channel (IKr) and the slow delayed rectifier potassium channel (IKs) in animal models with AF.
出处 《中华心律失常学杂志》 2005年第6期445-448,共4页 Chinese Journal of Cardiac Arrhythmias
关键词 心房颤动 电重构 延迟整流钾通道 基因表达 Atrial fibrillation Electrical remodeling Delayed rectifier potassium channels Gene expression
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参考文献12

  • 1Wijffels MC, Kirchhof C J, Dorland R, et al. Atrial fibrillation begets atrial fibrillation: a study in awake chronically instrumented goats. Circulation, 1995,92 : 1954-1968.
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二级参考文献13

  • 1Wijffels MC,Kirchhof CJ,Dorland R,et al.Atrial fibrillation begets Atrial fibrillation.A study in awake chronically instrumented goats.Circulation,1995,92:1954-1968.
  • 2Daoud EG,Bogun G,Goyal R,et al.Effect of AF on atrial refractoriness in humans.Circulation,1996,94:1600-1668.
  • 3Yue L,Feng J,Gaspo R,et al.Ionic remodding underlying action potential changes in a canine model of atrial fibrillation.Circ Res.1997,81:512-525.
  • 4Bosch RF,Zeng X,Grammer YB,et al.Ionic mechanisms of electrical remodeling in human atrial fibrillation.Cardiovasc Res,1999,44:121-131.
  • 5Van Wagoner DR,Pond AL,Lamorgese M,et al.Atrial L-type Ca2+ currents and human atrial fibrillation.Circ Res,1999,85:428-436.
  • 6Yue L,Melnyk P,Gaspo R,et al.Molecular mechanisms underlying ionic remodeling in a dog model of atrial fibrillation.Circ Res,1999,84:776-784.
  • 7Lai LP,Su MJ,Lin JL,et al.Down-regulation of L-type calcium channel and sarcopasmic reticular Ca2+ -ATPase mRNA in Human atrial fibrillation without significant change in the mRNA of ryanocine receptor,calsequestrin and phospholamban-an insight into the mechanism of atrial electrical remodeling.JACC,1999,33:1231-1237.
  • 8Brundel BJJM,Van Gelder IC,Henning RH,et al.Gene expression of proteins influencing calcium homeostasis in patients with persistent and paroxysmal atrial fibrillation.Cardiovas Res,1999,42:443-454.
  • 9Cheng TH,Lee FY,Wei J,et al.Comparison of calciumcurrent in isolated atrial myocytes from failing and nonfailing human hearts.Mol Cell Biochem,1996,157:157-162.
  • 10Boixel C,Gonzalez W,Louedec L,et al.Mechanisms of L-type Ca2+ current downregulation in rat atrial myocytes during heart failure.Circ Res,2001,89:607-613.

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