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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ca~(2+) oscillation frequency decoding in cardiac cell hypertrophy: Role of calcineurin/NFAT as Ca~(2+) signal integrators
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Ca~(2+) oscillation frequency decoding in cardiac cell hypertrophy: Role of calcineurin/NFAT as Ca~(2+) signal integrators

机译：Ca〜（2+）振荡频率解码在心肌肥大中的作用：钙调神经磷酸酶/ NFAT作为Ca〜（2+）信号整合剂的作用

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摘要

The role of Ca~(2+) signaling in triggering hypertrophy was investigated in neonatal rat cardiomyocytes in vitro. We show that an increase in cell size and sarcomere reorganization were elicited by receptor agonists such as Angiotensin II, aldosterone, and norepi-nephrine and by a small rise in medium KCI concentration, a treatment devoid of direct effects on receptor functions. All these treatments increased the frequency of spontaneous [Ca~(2+)] transients, caused nuclear translocation of transfected NFAT(GFP), and increased the expression of a NFAT-sensitive reporter gene. There was no increase in Ca~(2+) spark frequency in the whole cell or in the perinuclear region under these conditions. Hypertrophy and NFAT translocation but not the increased frequency of [Ca~(2+)] transients were inhibited by the calcineurin inhibitor cyclosporine A. Hypertrophy by the different stimuli was insensitive to inhibition of myofilament contraction. We concluded that calcineurin-NFAT can act as integrators of the contractile Ca~(2+) signal, and that they can decode alterations in the frequency even of rapid Ca~(2+) oscillations.
机译：体外研究了新生大鼠心肌细胞中Ca〜（2+）信号在触发肥大中的作用。我们表明，受体激动剂（例如血管紧张素II，醛固酮和去甲肾上腺素）和中等KCI浓度的小幅上升会引起细胞大小的增加和肌节结构的改变，以及中度KCI浓度的升高，这对受体功能没有直接影响。所有这些处理增加了自发的[Ca〜（2+）]瞬变的频率，引起了转染的NFAT（GFP）的核易位，并增加了NFAT敏感的报告基因的表达。在这些条件下，整个细胞或核周区域中的Ca〜（2+）火花频率均没有增加。钙调神经磷酸酶抑制剂环孢素A抑制肥大和NFAT易位，但不抑制[Ca〜（2+）]瞬变的频率增加。不同刺激引起的肥大对抑制肌丝收缩不敏感。我们得出的结论是，钙调神经磷酸酶-NFAT可以充当收缩Ca〜（2+）信号的积分器，并且即使在Ca〜（2+）快速振荡的情况下，它们也可以解码频率的变化。

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