Signal transduction of physiological cardiac hypertrophy

我们之前的研究表明，钙调磷酸酶在自愿运动训练引起的生理性左心室肥厚（LVH）中被激活，但在失代偿性压力过载的LVH中没有被激活。在目前的研究中，我们进一步研究了自愿运动诱导的LVH与压力过载LVH之间的差异，并将其转化为其他几种与肥厚相关的物质，包括小窝蛋白。Wistar大鼠被分配到以下三组中的一组：10周的自愿运动（EX），静坐方案（SED）和4周的升主动脉收缩（AC）。EX大鼠自愿跑1.6±1。1公里/天的特殊制造的笼子导致LVH（左心室重量/体重比增加24%）。EX大鼠心肌组织匀浆的肥大信号转导表现出与AC大鼠不同的特点。通过RNA保护实验，EX大鼠SR Ca^2+ATPase mRNA水平正常，肌球蛋白重链同工酶谱正常，AC大鼠SR Ca^2+ATPase mRNA水平降低，β肌球蛋白重链mRNA水平升高。Western blotting检测的心肌小室蛋白-3水平在EX大鼠中升高，而在AC大鼠中降低。自主运动诱导的LVH在信号转导上与失代偿的压力过载LVH不同。自律性运动诱导LVH诱导Caveolin-3，失代偿压力过载LVH诱导Caveolin-3降低。

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.