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首页> 外文期刊>Molecular biology reports >LncRNA MIAT/miR-133a-3p axis regulates atrial fibrillation and atrial fibrillation-induced myocardial fibrosis
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LncRNA MIAT/miR-133a-3p axis regulates atrial fibrillation and atrial fibrillation-induced myocardial fibrosis

机译：LNCRNA miat / mir-133a-3p轴调节心房颤动和心房颤动诱导的心肌纤维化

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摘要

Atrial fibrillation (AF) is a commonly encountered heart arrhythmia and a risk factor for cardiovascular system. The purpose of the present study was to explore the role of long non-coding RNA myocardial infarction-associated transcript (MIAT) in AF and AF-induced myocardial fibrosis and the possible mechanisms involved in this process. We successfully induced an AF rat model. Expression of MIAT presented a dramatic increase, while microRNA (miR)-133a-3p presented a dramatic decrease in atrium tissues of rats with AF induction. In addition, we also found that MIAT was highly expressed and miR-133a-3p was significantly reduced in peripheral blood leukocyte of AF patients. For biological function exploration of MIAT/miR-133a-3p axis, MIAT was knocked down using small hairpin RNA (shRNA) lentivirus injection and the rescue experiments were performed simultaneously by inhibiting miR-133a-3p using anti-miR-133a-3p lentivirus injection in rats with AF. MIAT downregulation significantly alleviated AF, increased atrial effective refractory period (AERP), and reduced the duration of AF as well as cardiomyocytes apoptosis. Whereas these effects of MIAT downregulation on AF were reversed by anti-miR-133a-3p administration. Luciferase reporter revealed that miR-133a-3p was directly regulated by MIAT. Moreover, MIAT knockdown effectively reduced AF-induced atrial fibrosis by detecting reduced collagen in the right atria and inhibited expression of fibrosis-related gene expression of collagen I, collagen III, connective tissue growth factor (CTGF) and transforming growth factor-beta 1 (TGF-beta 1) in rats with AF, these findings were in contrast with the findings for rats with inhibition of miR-133a-3p. In conclusion, our study demonstrated the role of MIAT downregulation in alleviating AF and AF-induced myocardial fibrosis, and the functional regulatory pathway of MIAT targeting miR-133a-3p.
机译：心房颤动（AF）是一种常见的心血炎和心血管系统的危险因素。本研究的目的是探讨长期非编码RNA心肌梗死相关转录物（MIAI）在AF和AF诱导的心肌纤维化中的作用以及该过程中所涉及的可能机制。我们成功诱导了AF大鼠模型。 MIAI的表达提出了显着的增加，而MicroRNA（miR）-133a-3p呈现了痤疮诱导大鼠的心室组织的显着降低。此外，我们还发现MIAI AIA is高表达，AF患者的外周血白细胞中MIR-133A-3P显着降低。对于Miat / miR-133a-3p轴的生物功能探索，使用小型发夹RNA（shRNA）慢敏虫液注射液体撞击，并且通过抗miR-133a-3p慢病毒抑制miR-133a-3p同时进行救援实验用AF的大鼠注射。寿命下调显着缓解了AF，心房有效耐火期（AERP）增加，降低了AF以及心肌细胞的持续时间。虽然这些抗MIR-133A-3P给药逆转了MIAI的这些对AF的影响。荧光素酶记者显示MIR-133A-3P是由MIAT直接调节的。此外，MIAI AIAI AIAI AT敲低通过检测右教中的降低的胶原蛋白，抑制胶原I，胶原III，结缔组织生长因子（CTGF）和转化生长因子-β1的纤维化相关基因表达表达和转化生长因子-β1（ TGF-β1）在AF的大鼠中，这些发现与抑制miR-133a-3p的大鼠的结果相反。总之，我们的研究表明了MIAI的作用下调在减轻AF和AF诱导的心肌纤维化中，以及靶向miat-133a-3p的模型功能调节途径。

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