Adenovirus-mediated overexpression of cardiac troponin I-interacting kinase promotes cardiomyocyte hypertrophy
Adenovirus-mediated overexpression of cardiac troponin I-interacting kinase promotes cardiomyocyte hypertrophy
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腺病毒介导的心肌肌钙蛋白 I 相互作用激酶过度表达促进心肌细胞肥大
DOI：
10.1111/j.1440-1681.2011.05499.x
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发表时间：
2011-04-01
影响因子：
2.9
通讯作者：
Meng, Xian-Min
中科院分区：
文献类型：
--
作者：
Wang, Lin;Wang, Hui;Meng, Xian-Min
P> 1。心肌肌钙蛋白I相互作用激酶（TNNI3K）是一种新的心肌特异性激酶基因。实时荧光定量逆转录聚合酶链反应分析显示，在内皮素-1（ET-1）诱导的肥大心肌细胞中，TNNI3K mRNA的表达显著增加。本研究旨在探讨TNNI3K对ET-1.2诱导的乳鼠心肌细胞肥大的影响。在293A细胞中扩增腺病毒。为了确定腺病毒感染心肌细胞的合理剂量，用携带人TNNI3K的腺病毒（Ad-TNNI3K）以不同的感染复数（MOI）感染心肌细胞，并通过western blot分析TNNI3K的表达.用携带绿色荧光蛋白的对照腺病毒（Ad-GFP）或Ad-TNNI3K感染心肌细胞。与Ad-GFP相比，Ad-TNNI3K可诱导肌节结构、细胞表面积、3H-Leu掺入和β-MHC重表达增加。这种类型的肥大现象类似于在Ad-GFP感染的由ET-1诱导的肥大心肌细胞中观察到的肥大现象。为了确定TNNI3K在ET-1诱导的肥大心肌细胞中的功能作用，用Ad-GFP或Ad-TNNI3K感染细胞。与Ad-GFP相比，Ad-TNNI3K可诱导肌节结构、细胞表面积和3H-亮氨酸掺入增加。这些结果表明，TNNI3K过表达诱导心肌细胞肥大并加速肥大心肌细胞的肥大。因此，TNNI3K可能是临床治疗肥大的一个有趣的靶点。
P>1. Cardiac troponin I-interacting kinase (TNNI3K) is a novel cardiac-specific kinase gene. Quantitative real-time reverse transcription polymerase chain reaction analysis showed a significant increase in TNNI3K mRNA expression in hypertrophic cardiomyocytes induced by endothelin-1 (ET-1). The aim of the present study was to investigate the effects of TNNI3K on neonate rat cardiomyocyte hypertrophy induced by ET-1.2. Adenoviruses were amplified in 293A cells. To determine a reasonable adenovirus infection dose cardiomyocytes were infected with an adenovirus carrying human TNNI3K (Ad-TNNI3K) at varying multiplicity of infection (MOI) and the expression of TNNI3K was analysed by western blot.3. Cardiomyocytes were infected with either a control adenovirus carrying green fluorescent protein (Ad-GFP) or Ad-TNNI3K. Compared with Ad-GFP, the Ad-TNNI3K induced an increase in sarcomere organization, cell surface area, 3H-leucine incorporation and beta-MHC re-expression. This type of hypertrophic phenomenon is similar to that observed in Ad-GFP-infected hypertrophic cardiomyocytes induced by ET-1. To determine the functional role of TNNI3K in ET-1-induced hypertrophic cardiomyocytes, the cells were infected with Ad-GFP or Ad-TNNI3K. Ad-TNNI3K induced an increase in sarcomere organization, cell surface area and 3H-leucine incorporation compared with Ad-GFP.4. These results suggest that TNNI3K overexpression induces cardiomyocytes hypertrophy and accelerates hypertrophy in hypertrophic cardiomyocytes. Therefore, TNNI3K might be an interesting target for the clinical treatment of hypertrophy.