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犬慢性心房颤动中 miR-133 和 miR-30 的表达。

Expression of miR-133 and miR-30 in chronic atrial fibrillation in canines.

机构信息

Department of Cardiology, College of Medicine, Shanghai Jiaotong University, Shanghai, People's Republic of China.

出版信息

Mol Med Rep. 2012 Jun;5(6):1457-60. doi: 10.3892/mmr.2012.831. Epub 2012 Mar 8.

DOI:10.3892/mmr.2012.831
PMID:22407060
Abstract

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. The most significant histological property of AF is atrial fibrosis, but the underlying mechanism is not clear. In this study we investigated the expression of miR-133 and miR-30, anti-fibrotic microRNAs (miRNAs), in chronic AF in canines. A total amount of 42 mongrel canines of either gender, weighing between 20 and 28 kg, were randomly assigned to the sham-operated and AF groups. All canines were subjected to weekly physical examinations and electrocardiogram. Alterations in tissue structure were assessed in atrial tissue samples by using hematoxylin and eosin and Masson's trichrome. The expression of miR-133 and miR-30 was determined by TaqMan real-time polymerase chain reaction (RT-PCR) and northern blot analyses of atrial tissue. The data were analyzed using the program SPSS 11.5 for Windows. At follow-up, rapid pacing from the left superior pulmonary vein induced sustained AF in the AF group. In the left atrium, increased interstitial fibrosis and chronic inflammation were observed. RT-PCR and northern blot analyses showed that miR-133 and miR-30 expression was downregulated in the AF group. Our results show that both miR-133 and miR-30 play an important role in controlling structural changes in chronic AF.

摘要

心房颤动(AF)是最常见的持续性心律失常。AF 的最显著组织学特性是心房纤维化,但潜在机制尚不清楚。在这项研究中,我们研究了犬慢性 AF 中抗纤维化 microRNA(miRNA)miR-133 和 miR-30 的表达。总共 42 只雄性和雌性杂种犬,体重在 20 到 28 公斤之间,随机分配到假手术组和 AF 组。所有犬每周进行体格检查和心电图检查。通过苏木精和伊红以及 Masson 三色染色评估心房组织样本中的组织结构变化。通过 TaqMan 实时聚合酶链反应(RT-PCR)和心房组织的 northern blot 分析确定 miR-133 和 miR-30 的表达。使用 Windows 版 SPSS 11.5 程序分析数据。随访时,从左上肺静脉快速起搏可在 AF 组中引起持续性 AF。在左心房中,观察到间质纤维化和慢性炎症增加。RT-PCR 和 northern blot 分析表明,miR-133 和 miR-30 在 AF 组中的表达下调。我们的结果表明,miR-133 和 miR-30 都在控制慢性 AF 中的结构变化方面发挥着重要作用。

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