Contractile activity and passive stretch regulate tubulin mRNA and protein content in cardiac myocytes.
Contractile activity and passive stretch regulate tubulin mRNA and protein content in cardiac myocytes.
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收缩活性和被动拉伸调节心肌细胞中微管蛋白 mRNA 和蛋白质含量。
DOI：
10.1152/ajpcell.1996.271.2.c684
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Giger,KE
中科院分区：
文献类型：
--
作者：
Watson,PA;Hannan,R;Carl,LL;Giger,KE
微管蛋白的积累和微管阵列的增加与体内压力过载后心肌细胞的收缩功能障碍有关。实验评估了在肥厚和扩张病理进展过程中心室心肌细胞所经历的机械刺激增加培养的新生大鼠心肌细胞β -微管蛋白产生的能力。结果表明，被动拉伸引起的收缩活性和负荷均通过β -微管蛋白mRNA的积累增加了新生大鼠心肌细胞中β -微管蛋白的含量，而β -微管蛋白基因转录并未增加。Western blot分析表明，收缩导致新生大鼠心肌细胞β -微管蛋白的积累，细胞总蛋白含量增加。Northern blot分析显示-微管蛋白mRNA含量随拉伸和收缩而增加。导致心肌细胞病理生理生长的α -肾上腺素能激动剂也刺激β -微管蛋白mRNA含量的增加。血管紧张素II （ANG II）治疗收缩的新生儿心肌细胞进一步增加β -微管蛋白mRNA含量，而ANG II治疗停滞的新生儿心肌细胞未能增加β -微管蛋白mRNA。核运行实验表明，收缩刺激β -微管蛋白mRNA积累，而不增加β -微管蛋白基因转录。这些结果表明，机械力可以直接调节培养心肌细胞的微管蛋白产生。在机械挑战的心脏中，β -微管蛋白的积累和收缩功能障碍的发展可能与心血管疾病发生和发展过程中施加在心肌上的机械力直接相关。
Accumulation of tubulin protein and an increased array of microtubules have been associated with contractile dysfunction in cardiac myocytes after pressure overload in vivo. Experiments were performed to assess the ability of mechanical stimuli experienced by ventricular cardiac myocytes during the progression of hypertrophic and dilated pathology to increase beta-tubulin production in cultured neonatal rat cardiac myocytes. Results indicate that both contractile activity and load due to passive stretch increase beta-tubulin protein content in neonatal rat cardiac myocytes through accumulation of beta-tubulin mRNA, which occurs without increased beta-tubulin gene transcription. Western blot analysis demonstrated that contraction resulted in the accumulation of beta-tubulin in neonatal rat cardiac myocytes above increases observed in the content of total cellular protein. Northern blot analysis indicated that beta-tubulin mRNA content increased in response to both stretch and contraction. alpha-Adrenergic agonists that lead to pathophysiological growth in cardiac myocytes also stimulated an increase in beta-tubulin mRNA content. Treatment of contracting neonatal cardiac myocytes with angiotensin II (ANG II) further increased beta-tubulin mRNA content, whereas ANG II treatment in arrested neonatal cardiac myocytes failed to increase beta-tubulin mRNA. Nuclear run-on experiments indicate that contraction stimulates beta-tubulin mRNA accumulation without an increase in beta-tubulin gene transcription. These results imply that tubulin production in cultured cardiac myocytes can be regulated directly by mechanical forces. In mechanically challenged hearts, the accumulation of beta-tubulin and the development of contractile dysfunction may be directly related to the mechanical forces imposed on the myocardium during the onset and progression of cardiovascular disease.
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