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首页> 外文期刊>European review for medical and pharmacological sciences. >miR-28 promotes cardiac ischemia by targeting mitochondrial aldehyde dehydrogenase 2 (ALDH2) in mus musculus cardiac myocytes
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miR-28 promotes cardiac ischemia by targeting mitochondrial aldehyde dehydrogenase 2 (ALDH2) in mus musculus cardiac myocytes

机译:miR-28通过靶向小家鼠心肌细胞中的线粒体醛脱氢酶2(ALDH2)促进心脏缺血

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OBJECTIVE: Aldehyde dehydrogenase 2 (ALDH2) is a crucial enzyme involved in protecting the heart from ischemic. MicroRNAs (miRNAs) are involved in gene down-regulation. However, this mechanism is unclear. The aim of this study was to investigate the role of miR-28 in the regulation of ALDH2 and to explore the mechanism of miR-28 in musculus of myocardial ischemia. MATERIALS AND METHODS: To evaluate the role of miR-28, we assessed cellular apoptosis. In addition, the regulation of ALDH2 by miR-199b was evaluated by Western blotting and luciferase assay. RESULTS: MiR-28 was up-regulated, while ALDH2 expression decreased in a time-dependent manner under normoxic conditions. The miR-28-transfected cells showed a significant decrease in the cellular apoptosis. Compared with the negative control 1 precursor molecules, miR-28 over-expression caused about 55% increase in myocardial apoptosis under hypoxic conditions, and miR-28 silencing by anti-miR-28 attenuated a 41% decreasing in apoptosis. MiR-28 and pGL3-ALDH2 vector-transfected cells showed that ALDH2 protein expression was suppressed and luciferase activity was reduced. CONCLUSIONS: These findings suggest that miR-28 promotes myocardial ischemia through the inhibition of ALDH2 expression in mus. miRNAs is as a probable index in identification of myocardial ischemia after acute myocardial infarction.
机译:目的:醛脱氢酶2(ALDH2)是一种重要的酶,可保护心脏免于缺血。 MicroRNA(miRNA)参与基因下调。但是,这种机制尚不清楚。这项研究的目的是调查miR-28在调节ALDH2中的作用,并探讨miR-28在心肌缺血小肌肉中的作用机制。材料与方法:为了评估miR-28的作用,我们评估了细胞凋亡。另外,通过蛋白质印迹和荧光素酶测定评估了miR-199b对ALDH2的调节。结果:在常氧条件下,MiR-28被上调,而ALDH2的表达则呈时间依赖性降低。经miR-28转染的细胞显示细胞凋亡明显减少。与阴性对照1前体分子相比,miR-28过表达导致缺氧条件下心肌细胞凋亡增加约55%,而抗miR-28引起的miR-28沉默可减轻41%的凋亡减少。转染了MiR-28和pGL3-ALDH2的细胞表明,ALDH2蛋白表达受到抑制,萤光素酶活性降低。结论:这些发现表明miR-28通过抑制小鼠中ALDH2的表达促进心肌缺血。 miRNA是鉴定急性心肌梗死后心肌缺血的可能指标。

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