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心房颤动犬中DDAH/PRMT/ADMA途径的变化

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

作者信息

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

机构信息

Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, PR China.

出版信息

Biochem Biophys Res Commun. 2008 Dec 19;377(3):884-8. doi: 10.1016/j.bbrc.2008.10.080. Epub 2008 Oct 23.

DOI:10.1016/j.bbrc.2008.10.080
PMID:18951871
Abstract

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 NO(X) 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.

摘要

心房颤动(AF)可能导致左心耳(LAA)内血栓形成。血栓形成与LAA心内膜功能障碍有关。由于不对称二甲基精氨酸(ADMA)可通过减少一氧化氮(NO)生成而导致内皮功能障碍,我们研究了AF犬的血浆ADMA和亚硝酸盐/硝酸盐(NO(X))水平以及心肌中二甲基精氨酸二甲胺水解酶-2(DDAH-2)、蛋白精氨酸甲基转移酶-1(PRMT-1)和内皮型一氧化氮合酶(eNOS)的蛋白含量。结果显示,血浆ADMA水平显著升高,血浆NO(X)浓度显著降低。与正常心脏相比,颤动心房中的DDAH-2表达未发生变化。然而,颤动心房中的DDAH活性显著降低。PRMT-1在LAA和左心房(LA)中的表达显著增加。LA中的eNOS表达显著降低。右心房中的eNOS和PRMT-1表达未发生变化。我们的结果表明,DDAH-PRMT-ADMA系统可能在调节AF中的内皮功能方面起关键作用。

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