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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/27650


    標題: The actions of mdivi-1, an inhibitor of mitochondrial fission, on rapidly activating delayed-rectifier K+ current and membrane potential in HL-1 murine atrial cardiomyocytes
    作者: So, Edmund Cheung
    Hsing, Chung-Hsi
    Liang, Chia-Hua
    Wu, Sheng-Nan
    Wu, Sheng-Nan�
    貢獻者: 化妝品應用與管理系
    關鍵字: Inhibitor Of Mitochondrial Division
    Rapidly Activating K+ Current
    Muscarinic K+ Channel
    Cardiomyocyte
    日期: 2012-05-15
    上傳時間: 2014-03-21 16:16:28 (UTC+8)
    出版者: Elsevier Science Bv
    摘要: Mdivi-1 is an inhibitor of dynamin related protein 1-(drp1)-mediated mitochondrial fission. However, the mechanisms through which this compound interacts directly with ion currents in heart cells remain unknown. In this study, its effects on ion currents and membrane potential in murine HL-1 cardiomyocytes were investigated. In whole-cell recordings, the addition of mdivi-1 decreased the amplitude of tail current (I-tail) for the rapidly activating delayed-rectifier K+ current (I-Kr) in a concentration-dependent manner with an IC50 value at 11.6 mu M, a value that resembles the inhibition requirement for mitochondrial division. It shifted the activation curve of I-tail to depolarized voltages with no change in the gating charge. However, mdivi-1 did not alter the rate of recovery from current inactivation. In cell-attached configuration, mdivi-1 inside the pipette suppressed the activity of acetylcholine-activated K+ channels without modifying the single-channel conductance. Mdivi-1 (30 mu M) slightly depressed the peak amplitude of Na+ current with no change in the overall current-voltage relationship. Under current-clamp recordings, addition of mdivi-1 resulted in prolongation for the duration of action potentials (APs) and to increase the firing of spontaneous APs in HL-1 cells. Similarly, in pituitary GH(3) cells, mdivi-1 was effective in directly suppressing the amplitude of ether-a-go-go-related gene-mediated K+ current. Therefore, the lengthening of AP duration and increased firing of APs caused by mdivi-1 can be primarily explained by its inhibition of these K+ channels enriched in heart cells. The observed effects of mdivi-1 on ion currents were direct and not associated with its inhibition of mitochondrial division. (C) 2012 Elsevier B. V. All rights reserved.
    關聯: European Journal of Pharmacology, 683(1-3), 1-9
    Appears in Collections:[化妝品應用與管理系(所)] 期刊論文

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