Signal transduction of physiological cardiac hypertrophy

我们以前的研究表明，钙调神经磷酸酶在自愿运动训练诱导的生理性左心室肥厚（LVH）中被激活，但在失代偿性压力超负荷LVH中没有激活。在目前的研究中，我们推进了我们的搜索自愿运动引起的LVH和压力超负荷LVH到其他几个肥大相关的物质，包括小窝之间的差异。Wistar大鼠被分配到以下三组之一：10周的自愿运动（EX），牙齿方案（SED），和4周的升主动脉缩窄（AC）。EX大鼠自主跑动1.6 ± 1。1 km/天，导致LVH（左心室重量/体重比增加24%）。EX大鼠心肌组织匀浆显示出与AC不同的肥大信号转导特征。RNA保护实验显示，EX大鼠SR Ca^2+ ATP酶mRNA水平正常，肌球蛋白重链同工酶谱正常，而AC大鼠SR Ca^2+ ATP酶mRNA水平降低，β肌球蛋白重链mRNA水平升高。Western blotting检测心肌小窝蛋白-3水平在EX大鼠中升高，但在AC大鼠中降低。自主运动引起的LVH与失代偿性压力超负荷LVH在信号转导上不同。Caveolin-3在自主运动性LVH中表达上调，而在失代偿性压力超负荷LVH中表达下调。

We previously showed that calcineurin was activated in physiological left ventricular hypertrophy (LVH) induced by voluntary exercise training, but not in decompensated pressure-overload LVH. In the current study, we advanced our search for the differences between the voluntary exercise-induced LVH and the pressure-overload LVH into several other hypertrophy-related substances including caveolin. Wistar rats were assigned to one of the following three groups : 10 weeks of voluntary exercise (EX) , a dentary regimen (SED) , and a 4-week of ascending aortic constriction (AC). The EX rats voluntarily ran 1.6 ± 1. 1 km/day in the specially manufactured cages resulting in LVH ( 24 % increase in left ventricular weight per body weight ratio ). Myocardial tissue homogenate of the EX rats revealed different characteristics in signal transduction of hypertrophy from that of the AC. The EX rats had normal SR Ca^2+ATPase mRNA level and normal myosin heavy chain isozyme pattern assessed by RNA protection assay, while AC rats had decreased SR Ca^2+ATPase mRNA level and increased beta myosin heavy chain mRNA level. Myocardial caveolin-3 protein levels assessed by Western blotting increased in the EX rats but decreased in the AC rats. The voluntary exercise-induced LVH differed in signal transduction from the decompensated pressure-overload LVH. Caveolin-3 was induced in the voluntary exercise-induced LVH, while it was decreased in the decompensated pressure-overload LVH.