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肌纤基因调节因子(myofibrillogenesis regulator1,MR1)是首次从人体骨骼肌cDNA文库中分离得到的基因.以前的研究证明MR1能够介导血管紧张素Ⅱ(AngⅡ)诱导的体内外心肌肥厚效应,但相关分子机制有待进一步阐明.利用腺病毒载体在小鼠中沉默MR1表达,利用基因芯片对比检查了小鼠心肌基因表达谱的变化.结果发现,在AngⅡ诱导心肌肥厚的小鼠,沉默MR1前后出现明显的信号通路方面的变化和基因表达差异,其中沉默MR1后表达降低90%以上的基因有39个,而表达升高10倍以上的基因有5个.在这些基因中,对与心肌肥厚密切相关的基因进行了定量RT-PCR检测,以进一步验证基因芯片的结果,发现沉默MR1后HSP72和硫氧还蛋白1(Trx1)均表达升高,而钙调神经磷酸酶β(CnAβ)和β肌球蛋白(β-myosin)的基因表达则受抑制.这些信号通路和基因均与AngⅡ诱导的心肌肥厚有一定的关系,为揭示MR1在AngⅡ所致心肌肥厚中的作用和分子机制提供了新的证据.
Myofibrillogenesis regulator1 (MR1) is the first gene isolated from human skeletal muscle cDNA library.Previous studies have shown that MR1 can mediate angiotensin II (AngⅡ) -induced myocardial hypertrophy in vitro and in vivo, but related The molecular mechanism needs to be further elucidated.Using adenovirus vector to silence the expression of MR1 in mice and compare the change of gene expression profile in mice by gene microarray.Results showed that in the mice induced by AngⅡmyocardial hypertrophy, Of the changes in the signal pathways and gene expression differences, including the silence of MR1 expression decreased more than 90% of the genes were 39, while the expression of more than 10 times more genes in 5. Of these genes, and myocardial hypertrophy are closely related The results of gene chip showed that the expression of both HSP72 and thioredoxin 1 (Trx1) increased after silencing MR1, while calcineurin β (CnAβ) and β The gene expression of β-myosin is inhibited.These signaling pathways and genes are related to Ang Ⅱ-induced cardiac hypertrophy. To reveal the effect of MR1 on AngⅡ Hypertrophy and molecular mechanisms of action provides new evidence.