scholarly journals New Candidate Genes in Atrial Fibrillation Polymorphisms of the Alpha 2-Beta-Adrenoceptor and the Endothelial NO Synthase Genes in Atrial Fibrillation of Different Etiological Origins

10.5772/53527 ◽  
2013 ◽  
Author(s):  
Svetlana Nikulina ◽  
Vladimir Shulman ◽  
Ksenya Dudkina ◽  
Anna Chernova ◽  
Oksana Gavrilyuk
Keyword(s):  
Atrial Fibrillation ◽  
Candidate Genes ◽  
No Synthase ◽  
Beta Adrenoceptor ◽  
Endothelial No Synthase

YIA4 Genetic Risk Markers for Atrial Fibrillation Influence Allelic Expression of Nearby Candidate Genes

Heart ◽  
2014 ◽  
Vol 100 (Suppl 3) ◽  
pp. A123.2-A124
Author(s):  
Ruairidh Martin ◽  
Andrew Owens ◽  
Mauro Santibanez Koref ◽  
Bernard Keavney
Keyword(s):  
Atrial Fibrillation ◽  
Candidate Genes ◽  
Genetic Risk ◽  
Allelic Expression ◽  
Risk Markers

scholarly journals Endothelial NO Synthase-Dependent S-Nitrosylation of β-Catenin Prevents Its Association with TCF4 and Inhibits Proliferation of Endothelial Cells Stimulated by Wnt3a

2017 ◽  
Vol 37 (12) ◽  
Author(s):  
Ying Zhang ◽  
Rony Chidiac ◽  
Chantal Delisle ◽  
Jean-Philippe Gratton
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Transcriptional Activity ◽  
No Synthase ◽  
Endothelial Cell Proliferation ◽  
Dependent Manner ◽  
Endothelial No Synthase ◽  
Binding Interface ◽  
Critical Residue

ABSTRACT Nitric oxide (NO) produced by endothelial NO synthase (eNOS) modulates many functions in endothelial cells. S-nitrosylation (SNO) of cysteine residues on β-catenin by eNOS-derived NO has been shown to influence intercellular contacts between endothelial cells. However, the implication of SNO in the regulation of β-catenin transcriptional activity is ill defined. Here, we report that NO inhibits the transcriptional activity of β-catenin and endothelial cell proliferation induced by activation of Wnt/β-catenin signaling. Interestingly, induction by Wnt3a of β-catenin target genes, such as the axin2 gene, is repressed in an eNOS-dependent manner by vascular endothelial growth factor (VEGF). We identified Cys466 of β-catenin as a target for SNO by eNOS-derived NO and as the critical residue for the repressive effects of NO on β-catenin transcriptional activity. Furthermore, we observed that Cys466 of β-catenin, located at the binding interface of the β-catenin–TCF4 transcriptional complex, is essential for disruption of this complex by NO. Importantly, Cys466 of β-catenin is necessary for the inhibitory effects of NO on Wnt3a-stimulated proliferation of endothelial cells. Thus, our data define the mechanism responsible for the repressive effects of NO on the transcriptional activity of β-catenin and link eNOS-derived NO to the modulation by VEGF of Wnt/β-catenin-induced endothelial cell proliferation.

Association between endothelial NO synthase polymorphism (rs3918226) and arterial properties

2012 ◽  
Vol 7 (1) ◽  
pp. 54 ◽  
Author(s):  
Jitka Seidlerová ◽  
Jan Filipovský ◽  
Otto Mayer ◽  
Renata Cífková ◽  
Martin Pešta ◽  
...  
Keyword(s):  
No Synthase ◽  
Endothelial No Synthase
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