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首页> 外文期刊>Cardiovascular pathology: the official journal of the Society for Cardiovascular Pathology >Role of miRNA-1 in regulating connexin 43 in ischemia-reperfusion heart injury: a rat model
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Role of miRNA-1 in regulating connexin 43 in ischemia-reperfusion heart injury: a rat model

机译：miRNA-1在缺血再灌注心损伤中调节Connexin33中的作用：大鼠模型

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MiRNA-1 may participate in regulating ischemia-reperfusion injury (IRI) by affecting the expression and distribution of connexin 43 (Cx43). The aim of this study is to investigate miR-1 expression and its potential role in regulating Cx43 during ischemic postconditioning (IPOST) in a rat model. Fifty-five Wistar male rats were randomly divided into five groups: N, IR, IPOST, agomir-1, and antagomir-1 group. The hearts were perfused with the Langendorff system. The reperfusion arrhythmia (RA) and myocardial infarct size were observed and recorded. The miRNA-1 expression and the Cx43 expression and distribution were assessed by RT-PCR, immunoblotting, and immunohistochemistry. First, the RA score in the IR group was higher than that in the control group, whereas there was no difference between the IPOST and antagomir-1 groups. Second, the myocardial infarct size was larger in the agomir-1 than in the IPOST group; there was no difference between the antagomir-1 and the IPOST group. Third, the miRNA-1 expression increased by 78% in the agomir-1 group but decreased by 32% in the antagomir-1 group compared with the IPOST group. Fourth, compared with the Control group, the Cx43 expression in the IR group decreased, the Cx43 expression decreased in the agomir-1 group compared with the IPOST group. Fifth, the distribution of Cx43 was irregular and disorganized in the IR and agomir-1 groups. In the IPOST and antagomir-1 groups, Cx43 was neatly distributed in the intercalated disk area. Our findings suggest that IPOST can inhibit the up-regulation of miRNA-1 induced by ischemia-reperfusion and that the down-regulation of miRNA-1 can prevent the decrease and redistribution of Cx43, which will protect the heart from IRI. (C) 2017 Elsevier Inc. All rights reserved.
机译：MiRNA-1可以通过影响Connexin 43（CX43）的表达和分布来调节缺血再灌注损伤（IRI）。本研究的目的是探讨miR-1表达及其在大鼠模型中缺血后处理期间CX43的潜在作用。五十五个Wistar雄性大鼠随机分为五组：N，IR，IPOST，Agomir-1和Antagomir-1组。心脏与Langendorff系统灌输。观察和记录再灌注心律失常（RA）和心肌梗塞大小。通过RT-PCR，免疫印迹和免疫组织化学评估miRNA-1表达和CX43表达和分布。首先，IR组中的RA得分高于对照组中的RA得分，而iPost和angomir-1组没有差异。其次，在Agomard-1中的心肌梗塞尺寸比在iPost组中更大; Antagomir-1和iPost组之间没有区别。第三，在AgomiR-1组中，MiRNA-1表达增加了78％，但与IPOST组相比，Antagomir-1组中的32％降低了32％。第四，与对照组相比，IR组中的CX43表达降低，与近期求和群体相比，Agomir-1组中的CX43表达降低。第五，CX43的分布在IR和Agomir-1组中不规则和混乱。在iPost和Antagomir-1组中，CX43整齐地分布在插入磁盘区域中。我们的研究结果表明，iPost可以抑制缺血再灌注诱导的miRNA-1的上调，并且miRNA-1的下调可以防止CX43的降低和再分布，这将保护心脏来自IRI。 （c）2017年Elsevier Inc.保留所有权利。

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