南方医科大学学报

南方医科大学学报 ›› 2006, Vol. 26 ›› Issue (12): 1754-1756.

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KCNE2对Kv4.3通道功能的调节作用

刘杰； 邓建新； 潘秉兴； 黄巧冰；   

  1. 南方医科大学病理生理学教研室； 南方医科大学病理生理学教研室 广东广州510515； 广东广州510515；
  • 出版日期:2006-12-20 发布日期:2006-12-20
  • 基金资助:
    国家自然科学基金(30570418,30570940)~~

KCNE2 modulates the function of Kv4.3 channel

LIU Jie,DENG Jian-xin,PAN Bing-xing,HUANG Qiao-bing Department of Pathophysiology,Southern Medical University,Guangzhou 510515,China   

  1. 南方医科大学病理生理学教研室； 南方医科大学病理生理学教研室 广东广州510515； 广东广州510515；
  • Online:2006-12-20 Published:2006-12-20

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摘要： 目的研究KCNE2对人类心肌细胞瞬间外向钾电流的主要α亚基-Kv4.3功能的调节。方法通过基因转染技术将Kv4.3或Kv4.3与KCNE2cDNA转入COS-7细胞株,采用膜片钳全细胞记录方式记录通道电流。结果KCNE2对Kv4.3功能有明显调控作用:减小Kv4.3通道电流密度;Kv4.3单独表达组通道电流密度为375.13±112.87pA/pF(n=11),KCNE2与Kv4.3共表达组电流密度为152.96±33.71pA/pF(n=16);减慢Kv4.3通道激活和衰减,在+60mV电压刺激下通道激活达峰值的时间由4.82±0.32ms(n=11)延长至20.41±2.13ms(n=16),P<0.05;通道电压依赖性失活发生正向移位,半数失活电压由-53.62±1.24mV(n=8)移至-46.58±1.6mV(n=10);通道从失活中恢复的速度加快,恢复时间常数由193.43±17.98ms缩短137.71±18.29ms,(n=7,P<0.05)。结论KCNE2可能作为人类心肌细胞膜Kv4.3钾离子通道一个重要的辅助亚基-β亚基参与Ito通道功能的调节。 更多还原

Abstract: Objective To understand the role of KCNE2 in functional regulation of Kv4.3,the major α subunit of transient outward current(Ito)in human heart.Methods The cDNAs of Kv4.3 or Kv4.3 plus KCNE2 were transfected into COS-7 cells and 24-36 h after the transfection,the channel proteins were expressed in the surface membrane of the cells and the channel currents were recorded with patch-clamp technique in whole-cell mode.Results KCNE2 played an important role in modulating the channel function.The recorded current density was decreased in cells co-expressing KCNE2 and Kv4.3 to 152.96±33.71 pA/pF(n=16)as compared with Kv4.3-expressing cells with a mean current density of 375.13±112.87 pA/pF(n=11).At the recording voltage of 60 mV,KCNE2 increased the time to peak(TTP)of the current.TTP in only Kv4.3-expressing cells was 4.82±0.32 ms(n=11),significantly shorter than the TTP of 20.41±2.13 ms(n=16)in cells co-expressing Kv4.3 and KCNE2(P<0.05).In the presence of KCNE2,the voltage-dependent inactivation of Kv4.3 showed a positive shift.The voltage of half maximum inactivation(V0.5)was decreased significantly from-53.62±1.24 mV(n=8)in Kv4.3 group to-46.58±1.6 mV(n=10)in KCNE2 co-expression group(P<0.05).KCNE2 accelerated the recovery of the channel from inactivation,reducing the recovery time constant(τ)from 193.43±17.98 ms to 137.71±18.29 ms.Conclusion KCNE2 might serve as an important β subunit and play a role in the regulation of Ito function in human heart.

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