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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >Microtubule proliferation in right ventricular myocytes of rats with monocrotaline-induced pulmonary hypertension.
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Microtubule proliferation in right ventricular myocytes of rats with monocrotaline-induced pulmonary hypertension.

机译：苦瓜碱诱导的肺动脉高压大鼠右室心肌细胞中的微管增殖。

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Microtubules are components of the cardiac cytoskeleton that can proliferate in response to pressure-overload in animal and human heart failure. We wished to test whether there was a proliferation of the microtubule cytoskeleton in the right ventricle of rats with pulmonary hypertension induced by monocrotaline (MCT) and whether this contributed to contractile dysfunction. Male Wistar rats were injected with 60mg/kg of MCT in saline or an equivalent volume of saline (CON). MCT produced clinical signs of heart failure within 4weeks of injection. Expression of right ventricular mRNA for α-tubulin was measured by real-time reverse transcription polymerase chain reaction. Free and polymerised fractions of β-tubulin protein were assessed using Western blot analysis and immunofluorescence microscopy was used to assess tyrosinated and acetylated (stabilized) microtubules. Right ventricular myocyte contraction was measured in response to the microtubule de-polymeriser colchicine (10μmol/l for at least 1h). Compared to CON, in MCT right ventricles there was a small but statistically significant increase in the expression of mRNA for α-tubulin (P<0.001); total (P<0.05) and polymerised fraction (P<0.01) of β-tubulin protein and level of acetylated tubulin (P<0.01). However colchicine treatment did not increase the contraction of MCT myocytes (P>0.05) or affect their response to increased stimulation frequency. Our observations support the hypothesis that microtubule proliferation is a common response to pulmonary hypertension in failing right ventricles but suggest that the effect this has on contraction depends upon the specific experimental or clinical conditions that prevail and the subsequent level of microtubule proliferation.
机译：微管是心脏细胞骨架的组成部分，可响应动物和人类心力衰竭中的压力超负荷而增殖。我们希望测试一丁二酚（MCT）诱发的肺动脉高压大鼠右心室是否存在微管细胞骨架的增殖，以及这是否导致了收缩功能障碍。向雄性Wistar大鼠注射60mg / kg的MCT盐水或等体积的盐水（CON）。 MCT在注射后4周内产生了心力衰竭的临床体征。通过实时逆转录聚合酶链反应检测α-微管蛋白的右心室mRNA表达。使用蛋白质印迹分析评估β-微管蛋白蛋白的游离级分和聚合级分，并使用免疫荧光显微镜评估酪氨酸化和乙酰化（稳定化）微管。响应微管解聚秋水仙碱（10μmol/ l持续至少1h），测量右室心肌细胞的收缩。与CON相比，MCT右心室中α-微管蛋白的mRNA表达略有增加，但具有统计学意义（P <0.001）。 β-微管蛋白的总含量（P <0.05）和聚合级分（P <0.01）和乙酰化微管蛋白的水平（P <0.01）。然而秋水仙碱治疗并没有增加MCT心肌细胞的收缩（P> 0.05）或影响其对增加刺激频率的反应。我们的观察结果支持以下假设，即微管增生是右心衰竭时对肺动脉高压的常见反应，但提示其对收缩的影响取决于普遍存在的特定实验或临床条件以及随后的微管增生水平。

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