| Variance of DDAH/PRMT/ADMA pathway in atrial fibrillation dogs. | |
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MedLine Citation:
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PMID: 18951871 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Hongyan Liu; Xiufen Qu; Zhaoguang Liang; Weiye Chen; Wei Xia; Ying Song |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-10-23 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: 377 ISSN: 1090-2104 ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2008 Dec |
Date Detail:
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Created Date: 2008-11-25 Completed Date: 2008-12-15 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
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Languages: eng Pagination: 884-8 Citation Subset: IM |
Affiliation:
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Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin 150001, PR China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amidohydrolases
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blood,
metabolism* Animals Arginine / analogs & derivatives*, blood, metabolism Atrial Fibrillation / blood, complications, enzymology* Disease Models, Animal Dogs Down-Regulation Endothelium / enzymology Female Male Myocardium / enzymology Nitric Oxide / blood Nitric Oxide Synthase Type II / antagonists & inhibitors, metabolism Nitric Oxide Synthase Type III / antagonists & inhibitors, metabolism Protein-Arginine N-Methyltransferases / blood, metabolism* Thrombosis / enzymology*, etiology Up-Regulation |
| Chemical | |
Reg. No./Substance:
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0/dimethylarginine; 10102-43-9/Nitric Oxide; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 2.1.1.-/Protein-Arginine N-Methyltransferases; EC 3.5.-/Amidohydrolases; EC 3.5.3.18/dimethylargininase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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