Variance of DDAH/PRMT/ADMA pathway in atrial fibrillation dogs

文献类型： 外文期刊

第一作者： Liu, Hongyan

作者： Liu, Hongyan;Qu, Xiufen;Liang, Zhaoguang;Xia, Wei;Song, Ying;Chen, Weiye

作者机构：

关键词： Atrial fibrillation;Asymmetric dimethylarginine;Dimethylarginine dimethylaminohydrolase;Endothelial dysfunction;Nitric oxide;Nitric oxide synthase;Oxidative stress;Protein arginine methyltransferase

期刊名称：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS （ 影响因子：3.575； 五年影响因子：3.381 ）

ISSN： 0006-291X

年卷期： 2008 年 377 卷 3 期

页码：

收录情况： SCI

摘要： Atrial fibrillation (AF) may cause thrombus formation in the left atrial appendage (LAA). Thrombus formation is associated with LAA endocardial dysfunction. Because asymmetrical dimethylarginine (ADMA) can cause endothelial dysfunction by decreasing nitric oxide (NO) formation, we investigated plasma ADMA and nitrite/nitrate (NO(x)) levels and myocardial dimethylarginine dimethylaminohydrolase-2 (DDAH-2), Protein arginine methyltransferase-1 (PRMT-1), and endothelial NO synthase (eNOS) protein contents from AF dogs. The results displayed that plasma ADMA level significantly increased, and plasma NOx concentration significantly decreased. Compared with normal heart, DDAH-2 expression was unchanged in the fibrillating atria. However, the DDAH activity was significantly decreased in the fibrillating atria. PRMT-1 expression significantly increased in the LAA and in the left atrium (LA). ENOS expression significantly decreased in the LA. ENOS and PRMT-1 expressions were unchanged in the right atria. Our results suggested that the DDAH-PRMT-ADMA system maybe play a pivotal role in regulating endothelial function in AF. (C) 2008 Elsevier Inc. All rights reserved.

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