Regulation of Endothelial No Synthase Activity by Estrogen Receptors in a Steroid Receptor Fast-Action Complex (SRFC) in Caveolae

2003 ◽  
pp. 27-35
Author(s):  
Philip W. Shaul ◽  
Ken L. Chambliss ◽  
Chieko Mineo
Keyword(s):  
Estrogen Receptors ◽  
Steroid Receptor ◽  
No Synthase ◽  
Endothelial No Synthase

scholarly journals Expression of Endothelial NO Synthase, Inducible NO Synthase, and Estrogen Receptors Alpha and Beta in Placental Tissue of Normal, Preeclamptic, and Intrauterine Growth-restricted Pregnancies

2005 ◽  
Vol 53 (12) ◽  
pp. 1441-1449 ◽  
Author(s):  
Barbara Schiessl ◽  
Ioannis Mylonas ◽  
Peer Hantschmann ◽  
Christina Kuhn ◽  
Sandra Schulze ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Western Blot ◽  
Estrogen Receptors ◽  
Placental Tissue ◽  
No Synthase ◽  
Trophoblast Cells ◽  
Expression Intensity ◽  
Intrauterine Growth ◽  
Endothelial No Synthase ◽  
Inducible No Synthase

In the physiology of placental blood circulation, nitric oxide (NO) synthases seem to play important roles, although their expression in pathological placentas and their role is still unclear. In addition, NO synthase activation seems to be related to estrogen receptor expression. Therefore, the aims of this study were to investigate the expression of estrogen receptors alpha (ERα), estrogen receptor beta (ER and the endothelial NO synthase (eNOS), and inducible NO synthase (iNOS) in intrauterine growth-restricted (IUGR) placentas, preeclamptic placentas, and in normal healthy control placentas. Slides of paraffin-embedded placental tissue were obtained after delivery from patients diagnosed with IUGR, preeclampsia, and normal term placentas and analyzed for eNOS, iNOS as well as ERα and ERβ expression. Intensity of immunohistochemical reaction was analyzed using a semiquantitative score and statistical analysis was performed. In addition, Western blot experiments were performed for comparison of staining intensities obtained by immunohis-tochemistry and western blot. Expression of eNOS, iNOS, and ERβ is significantly reduced in trophoblast cells of placentas with IUGR. However, preeclamptic placentas demonstrated a significant elevated expression intensity of these proteins compared with normal controls. A different expression of eNOS, iNOS, ERα, and ERβ by human trophoblast cells seems to results in lower NO output and impaired trophoblast invasion. Results obtained in our study provide evidence that reduced expression of the investigated proteins is related to IUGR.

Role of single nucleotide Т786C polymorphism of endothelial NO-synthase gene after myocardial infarction with ST-segment elevation

2019 ◽  
Vol 0 (2) ◽  
pp. 63-72
Author(s):  
O. V. Petyunina ◽  
M. P. Kopytsya ◽  
A. E. Berezin ◽  
D. P. Babichev
Keyword(s):  
Myocardial Infarction ◽  
No Synthase ◽  
Single Nucleotide ◽  
St Segment Elevation ◽  
Endothelial No Synthase ◽  
St Segment

scholarly journals Endothelial NO Synthase Gene Polymorphisms and Risk of Ischemic Stroke in Asian Population: A Meta-Analysis

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e60472 ◽  
Author(s):  
Meiyun Wang ◽  
Xiubo Jiang ◽  
Wenlong Wu ◽  
Dongfeng Zhang
Keyword(s):  
Ischemic Stroke ◽  
Gene Polymorphisms ◽  
Meta Analysis ◽  
Asian Population ◽  
No Synthase ◽  
Endothelial No Synthase

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.

scholarly journals Activated Platelets from Diabetic Rats Cause Endothelial Dysfunction by Decreasing Akt/Endothelial NO Synthase Signaling Pathway

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e102310 ◽  
Author(s):  
Keiko Ishida ◽  
Kumiko Taguchi ◽  
Takayuki Matsumoto ◽  
Tsuneo Kobayashi
Keyword(s):  
Endothelial Dysfunction ◽  
Signaling Pathway ◽  
Diabetic Rats ◽  
No Synthase ◽  
Endothelial No Synthase ◽  
Activated Platelets
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