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首页> 外文OA文献 >The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes.
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The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes.

机译：心脏β-肌球蛋白重链同基因在培养的大鼠心脏心肌细胞的α1-肾上腺素受体刺激的肥大中被选择性诱导。

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Cardiac hypertrophy produced in vivo by pressure overload is characterized by selective up-regulation of the fetal/neonatal beta-cardiac myosin heavy chain (MHC) isogene. However, a molecular signal for beta-MHC isogene induction has not been identified. We examined cardiac MHC isogene expression in a cell culture model for hypertrophy. alpha-MHC and beta-MHC iso-protein and iso-mRNA levels in cultured cardiac myocytes were quantified during hypertrophy stimulated by the alpha 1-adrenergic agonist, norepinephrine (NE). beta-MHC iso-protein content was increased 3.2-fold vs. control (P less than 0.001), whereas alpha-MHC isoprotein content was not changed significantly (1.4-fold vs. control, P = NS). MHC iso-mRNA levels were quantified by nuclease S1 analysis, using a single oligonucleotide probe. NE increased beta-MHC iso-mRNA content by 3.9-fold vs. control (P less than 0.001), but there was no change in alpha-MHC iso-mRNA (1.1-fold vs. control, P = NS). The NE-stimulated increase in beta-MHC iso-mRNA preceded in time the increase in beta-MHC isoprotein accumulation. The EC50 for NE induction of beta-MHC was 40 nM, and pharmacologic experiments indicated alpha 1-adrenergic receptor specificity. alpha-MHC isogene expression was predominant in control myocytes (68% alpha-isoprotein and 60% alpha-iso-mRNA). In contrast, beta-MHC expression was equal to alpha-MHC or predominant after treatment with NE (51% beta-isoprotein and 69% beta-iso-mRNA). Thus, alpha 1-adrenergic receptor stimulation increases the cellular contents of beta-MHC iso-mRNA and beta-MHC isoprotein during hypertrophy of cultured neonatal rat cardiac myocytes, but does not change the levels of alpha-MHC iso-mRNA or isoprotein. The effect on beta-MHC is mediated primarily at the level of mRNA steady-state level (pretranslational). Activation of the alpha 1-adrenergic receptor is the first identified molecular signal for increased beta-MHC isogene expression in a model of cardiac hypertrophy.
机译：由压力超负荷在体内产生的心脏肥大的特征在于胎儿/新生儿β-心脏肌球蛋白重链（MHC）同基因的选择性上调。但是，尚未确定β-MHC同基因诱导的分子信号。我们检查了肥大细胞培养模型中心脏MHC同基因的表达。在由α1-肾上腺素能激动剂去甲肾上腺素（NE）刺激的肥大过程中，对培养的心肌细胞中的α-MHC和β-MHC异蛋白和iso-mRNA水平进行了定量。与对照组相比，β-MHC异蛋白含量增加了3.2倍（P小于0.001），而与对照相比，α-MHC异蛋白含量没有明显变化（与对照组相比，增加了1.4倍，P = NS）。使用单个寡核苷酸探针通过核酸酶S1分析定量MHC iso-mRNA水平。 NE使beta-MHC iso-mRNA含量比对照增加了3.9倍（P小于0.001），但alpha-MHC iso-mRNA没有变化（与对照相比，1.1倍，P = NS）。 NE刺激的beta-MHC异构mRNA的增加先于beta-MHC异构蛋白积累的增加。 NE诱导β-MHC的EC50为40 nM，药理实验表明α1-肾上腺素能受体特异性。 α-MHC同基因表达在对照心肌细胞中占主导地位（68％的α-异蛋白和60％的α-iso-mRNA）。相反，β-MHC表达等于α-MHC或以NE治疗后占主导地位（51％β-异蛋白和69％β-iso-mRNA）。因此，在培养的新生大鼠心肌细胞肥大过程中，α1-肾上腺素能受体刺激增加了β-MHC异型mRNA和β-MHC异型蛋白的细胞含量，但不会改变α-MHC异型mRNA或同型蛋白的水平。对β-MHC的影响主要在mRNA稳态水平（翻译前）上介导。 α1-肾上腺素能受体的激活是心脏肥大模型中第一个确定的增加β-MHC同基因表达的分子信号。

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