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.

Expression of Estrogen Receptor-α, Estrogen Receptor-β and Placental Endothelial and Inducible NO Synthase in Intrauterine Growth-Restricted and Normal Placentas

2006 ◽  
Vol 37 (8) ◽  
pp. 967-975 ◽  
Author(s):  
Barbara Schiessl ◽  
Ioannis Mylonas ◽  
Christina Kuhn ◽  
Susanne Kunze ◽  
Sandra Schulze ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
No Synthase ◽  
Estrogen Receptor Β ◽  
Intrauterine Growth ◽  
Inducible No Synthase

scholarly journals Striatin assembles a membrane signaling complex necessary for rapid, nongenomic activation of endothelial NO synthase by estrogen receptor  

2004 ◽  
Vol 101 (49) ◽  
pp. 17126-17131 ◽  
Author(s):  
Q. Lu ◽  
D. C. Pallas ◽  
H. K. Surks ◽  
W. E. Baur ◽  
M. E. Mendelsohn ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
No Synthase ◽  
Signaling Complex ◽  
Endothelial No Synthase ◽  
Membrane Signaling

Clinical factors such as B-type natriuretic peptide link to factor VII, endothelial NO synthase and estrogen receptor α polymorphism in elderly women

Life Sciences ◽  
2009 ◽  
Vol 85 (7-8) ◽  
pp. 316-321 ◽  
Author(s):  
Jun Funami ◽  
Toshio Hayashi ◽  
Hideki Nomura ◽  
Qun-Fang Ding ◽  
Asako Ishitsuka-Watanabe ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Natriuretic Peptide ◽  
Elderly Women ◽  
Estrogen Receptor Α ◽  
No Synthase ◽  
Factor Vii ◽  
Clinical Factors ◽  
Endothelial No Synthase

scholarly journals Variant estrogen receptor c-Src molecular interdependence and c-Src structural requirements for endothelial NO synthase activation

2007 ◽  
Vol 104 (42) ◽  
pp. 16468-16473 ◽  
Author(s):  
L. Li ◽  
K. Hisamoto ◽  
K. H. Kim ◽  
M. P. Haynes ◽  
P. M. Bauer ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
No Synthase ◽  
Structural Requirements ◽  
Endothelial No Synthase

Mechanisms of homocysteine-induced oxidative stress

2005 ◽  
Vol 289 (6) ◽  
pp. H2649-H2656 ◽  
Author(s):  
Neetu Tyagi ◽  
Kara C. Sedoris ◽  
Mesia Steed ◽  
Alexander V. Ovechkin ◽  
Karni S. Moshal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
No Synthase ◽  
Oxygen Species ◽  
Neuronal No Synthase ◽  
Endothelial No Synthase ◽  
Inducible No Synthase ◽  
Cardiovascular Morbidity And Mortality

Hyperhomocysteinemia decreases vascular reactivity and is associated with cardiovascular morbidity and mortality. However, pathogenic mechanisms that increase oxidative stress by homocysteine (Hcy) are unsubstantiated. The aim of this study was to examine the molecular mechanism by which Hcy triggers oxidative stress and reduces bioavailability of nitric oxide (NO) in cardiac microvascular endothelial cells (MVEC). MVEC were cultured for 0–24 h with 0–100 μM Hcy. Differential expression of protease-activated receptors (PARs), thioredoxin, NADPH oxidase, endothelial NO synthase, inducible NO synthase, neuronal NO synthase, and dimethylarginine-dimethylaminohydrolase (DDAH) were measured by real-time quantitative RT-PCR. Reactive oxygen species were measured by using a fluorescent probe, 2′,7′-dichlorofluorescein diacetate. Levels of asymmetric dimethylarginine (ADMA) were measured by ELISA and NO levels by the Griess method in the cultured MVEC. There were no alterations in the basal NO levels with 0–100 μM Hcy and 0–24 h of treatment. However, Hcy significantly induced inducible NO synthase and decreased endothelial NO synthase without altering neuronal NO synthase levels. There was significant accumulation of ADMA, in part because of reduced DDAH expression by Hcy in MVEC. Nitrotyrosine expression was increased significantly by Hcy. The results suggest that Hcy activates PAR-4, which induces production of reactive oxygen species by increasing NADPH oxidase and decreasing thioredoxin expression and reduces NO bioavailability in cultured MVEC by 1) increasing NO2-tyrosine formation and 2) accumulating ADMA by decreasing DDAH expression.

scholarly journals Enhanced production of nitric oxide by blood-dialysis membrane interaction.

1995 ◽  
Vol 6 (4) ◽  
pp. 1278-1283
Author(s):  
A Amore ◽  
R Bonaudo ◽  
D Ghigo ◽  
M Arese ◽  
C Costamagna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Fold Increase ◽  
No Synthase ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Endothelial No Synthase ◽  
Enhanced Production ◽  
Inducible No Synthase

Nitric oxide (NO) is a powerful vasoactive product of endothelial origin, and one of its major effects is vasodilation, leading to hypotension. The role of NO in some complications of uremia is still debated. This study evaluated whether endothelial NO synthase activity could be modulated by the exposure of healthy blood to hemodialysis materials. In vitro hemodialysis sessions were performed with cuprophan and polymethylmethacrylate membranes. Blood samples from a healthy donor after recirculation for 0, 5, 15, 30, and 60 min were coincubated for 6 h with a murine endothelial cell line (t.End.1); mRNA for inducible NO synthase and enzyme activity, measured as (3H)citrulline produced from (3H)arginine, were detected. The release of interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNF-alpha) from recirculating lymphomonocytes was measured, too. The NO synthase activity of endothelial cells was stimulated by blood dialyzed with cuprophan, peaking at 15 min (11-fold increase in comparison to the basal values), whereas polymethylmethacrylate was ineffective (P < 0.01 versus Cuprophan). Dialysis with cuprophan, but not with polymethylmethacrylate, induced in endothelial cells the expression of mRNA encoding for inducible NO synthase. The release of IL-1 beta and TNF-alpha after 6 h by recirculating lymphomonocytes paralleled the NO synthase activity profile in endothelial cells and was significantly higher after cuprophan exposure than after polymethylmethacrylate (P < 0.0001). In conclusion, the activity of endothelial NO synthase can be enhanced during the dialysis sessions by the interaction of lymphomonocytes with the membranes, possibly via TNF-alpha and IL-1 beta production.

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