Effect of ablation of phospholamban on dynamics of cardiac myocyte contraction and intracellular Ca2+.
Effect of ablation of phospholamban on dynamics of cardiac myocyte contraction and intracellular Ca2+.
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DOI：
10.1152/ajpcell.1996.271.1.c391
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发表时间：
1996-07
期刊：
影响因子：
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通讯作者：
B. Wolska;M. Stojanovic;W. Luo;E. G. Kranias;R. Solaro
中科院分区：
文献类型：
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作者：
B. Wolska;M. Stojanovic;W. Luo;E. G. Kranias;R. Solaro
我们比较了野生型和磷蛋白（PLB）缺陷小鼠心脏中分离的心室肌细胞在控制条件和β -肾上腺素能刺激下的机械活性和Ca2+瞬态。与野生型对照相比，从plb缺陷小鼠心脏分离的细胞显示1)细胞缩短程度增加2倍，2)最大缩短速度增加3倍，3)最大延长速度增加3.4倍。plb缺陷肌细胞也表现出fura 2荧光比的峰值幅度和Ca2+瞬态上升和下降相的速率显著增加。两组的fura 2舒张比相似，表明舒张期间细胞内Ca2+没有变化。在plb缺乏的肌细胞中，0.05 μ m异丙肾上腺素诱导抽搐幅度增加152 +/- 11% (n = 6)，而在野生型细胞中为290 +/- 31% （n = 6）。与野生型细胞的最大缩短速度398 +/- 62% （n = 6）相比，plb缺陷型细胞的最大缩短速度增加了183 +/- 10% （n = 6）。异丙肾上腺素诱导的最大再增强速度在plb缺陷细胞中增加了168 +/- 8% (n = 6)，而在野生型肌细胞中增加了445 +/- 71% （n = 6）。在两组中，这些收缩参数的变化都伴随着Ca2+瞬态的变化。我们的研究结果表明，PLB以外的磷酸化位点可能在心脏细胞响应β -肾上腺素能刺激的收缩-松弛动力学调节中发挥重要作用。
We compared mechanical activity and Ca2+ transients of ventricular myocytes isolated from wild-type and phospholamban (PLB)-deficient mouse hearts in control conditions and during beta-adrenergic stimulation. Compared with wild-type controls, cells isolated from PLB-deficient mouse hearts showed 1) a 2-fold increase in extent of cell shortening, 2) a 3-fold increase in maximal shortening velocity, and 3) a 3.4-fold increase in maximal relengthening velocity. PLB-deficient myocytes also demonstrated significant increases in the peak amplitude of the fura 2 fluorescence ratio and the rates of rising and falling phases of the Ca2+ transient. The fura 2 diastolic ratios were similar in both groups, suggesting no change in intracellular Ca2+ during diastole. In PLB-deficient myocytes, 0.05 microM isoproterenol induced an increase in the twitch amplitude by 152 +/- 11% (n = 6) compared with 290 +/- 31% (n = 6) in wild-type cells. Maximal shortening velocity was increased by 183 +/- 10% (n = 6) in PLB-deficient myocytes, compared with 398 +/- 62% (n = 6) in wild-type cells. The isoproterenol-induced increase in maximum relengthening velocity was increased by 168 +/- 8% (n = 6) in PLB-deficient cells compared with 445 +/- 71% (n = 6) in wild-type myocytes. In both groups, these changes in contractile parameters were accompanied by changes in the Ca2+ transient. Our results indicate that phosphorylation of sites other than PLB may play an important role in regulation of contraction-relaxation dynamics of heart cells responding to beta-adrenergic stimulation.