scholarly journals Decreased eNOS Protein Expression in Involuting and Propranolol-Treated Hemangiomas

2012 ◽  
Vol 138 (2) ◽  
pp. 177 ◽  
Author(s):  
Yuemeng Dai
Keyword(s):  
Protein Expression ◽  
Enos Protein Expression ◽  
Enos Protein

scholarly journals PI3K-Akt/eNOS in remote postconditioning induced by brief pulmonary ischemia

2014 ◽  
Vol 37 (1) ◽  
pp. 26 ◽  
Author(s):  
Yan-hua Tang ◽  
Jue-shen Yang ◽  
Hai-yan Xiang ◽  
Jia-jun Xu
Keyword(s):  
Protein Expression ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rabbit Model ◽  
Serum Levels ◽  
Myocardial Cells ◽  
Akt Inhibitor ◽  
Remote Postconditioning ◽  
Enos Protein Expression ◽  
Enos Protein

Purpose: Postconditioning, a series of brief ischemia-reperfusion sequences given before an ischemic heart undergoes sustained reperfusion, has been shown to lessen ischemia/reperfusion injury. The current study establishes a rabbit model of myocardial ischemia-reperfusion and studied the effects of pulmonary remote postconditioning in this model. Methods: Serum levels of creatine kinase (CK), superoxide dismutase (SOD), and malondialdehyde (MDA), protein expression of endothelial nitric oxide synthase (eNOS), Rho kinase (ROCK- 2), and protein kinase B (Akt) in myocardial cells and the apoptosis index of myocardial cells were examined. Results: Pulmonary remote postconditioning decreased CK, significantly decreased MDA, and increased SOD. Postconditioning significantly increased eNOS protein expression. Administration of eNOS inhibitor, L-NAME, dramatically suppressed the postconditioning-induced eNOS protein expression and serum SOD level, but significantly increased MDA level. The two longer sessions of postconditioning increased Akt, although this increase was not accompanied by changes in levels of the Akt inhibitor, ROCK-2. Blocking eNOS activity with L-NAME had no visible effect on either Akt or ROCK-2. Conclusion: Our results suggest a role for Akt in remote postconditioning-induced myocardial protection, but do not support an involvement of eNOS in Akt-mediated action.

Prolonged AMP-activated protein kinase induction impairs vascular functions

2013 ◽  
Vol 91 (12) ◽  
pp. 1025-1030 ◽  
Author(s):  
Saadet Turkseven ◽  
Elif Ertuna
Keyword(s):  
Protein Kinase ◽  
Protein Expression ◽  
Response Curves ◽  
Compound C ◽  
Amp Activated Protein Kinase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
The Impact ◽  
Enos Protein Expression ◽  
Enos Protein

AMP-activated protein kinase (AMPK) is a regulator of cellular metabolism and is involved in the pathogenesis of several diseases, including type 2 diabetes and cardiovascular diseases. Data showing the effects of AMPK on vasculature are controversial. Therefore, the aim of this study was to determine the impact of prolonged AMPK activation on vascular functions. For this purpose we have examined the role of AMPK in endothelium-dependent and -independent relaxation and vascular contractions. For this, we incubated thoracic aortic rings, from rats, with AMPK activator 5-aminoimidazole-4-carboxamide-1-4-ribofuranoside (AICAR, 500 μmol/L or 2 mmol/L) in the presence or absence of AMPK inhibitor compound C (10 μmol/L). Next, cumulative dose–response curves to acetylcholine (ACh) (10−9−10−4 mol/L), nitroglycerine (NG) (10−9–3 × 10−5 mol/L), and noradrenaline (NA) (10−9−10−4 mol/L) were obtained. Endothelial nitric oxide synthase (eNOS) protein expression was determined. Our results show that endothelium-dependent relaxation was inhibited after AICAR treatment, and that this effect was reversed by AMPK inhibition. Moreover, AICAR enhanced the contractile response to NA and caused a decrease in eNOS protein expression. In conclusion, prolonged AMPK induction causes endothelial impairment, possibly via increased degradation and (or) reduced expression of eNOS.

scholarly journals Activation of the Mitogen-Activated Protein Kinase Cascade Is Necessary But Not Sufficient for Basic Fibroblast Growth Factor- and Epidermal Growth Factor-Stimulated Expression of Endothelial Nitric Oxide Synthase in Ovine Fetoplacental Artery Endothelial Cells*

Endocrinology ◽  
1999 ◽  
Vol 140 (3) ◽  
pp. 1399-1407 ◽  
Author(s):  
Jing Zheng ◽  
Ian M. Bird ◽  
Amy N. Melsaether ◽  
Ronald R. Magness
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Growth Factor ◽  
Protein Expression ◽  
Mapk Cascade ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Enos Protein Expression ◽  
Enos Protein

Abstract Basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF) may play important roles in the placental vasculature, not only by controlling cell growth and differentiation, but also by mediating production of local vasodilators such as nitric oxide. As the mitogen-activated protein kinase (MAPK) signal cascade has been widely associated with cell growth in response to growth factors, herein we investigate whether bFGF, EGF, and VEGF also stimulate expression of endothelial nitric oxide synthase (eNOS) via activation of the MAPK cascade in ovine fetoplacental artery endothelial cells. The presence of the receptors for all three growth factors was confirmed by both immunocytochemistry and a functional cell proliferation assay. All three growth factors at 10 ng/ml rapidly (<10 min) activated MAPK. This activation was inhibited by PD 98059, a specific MAPK kinase inhibitor. bFGF and EGF, but not VEGF, dose- and time-dependently increased eNOS protein levels. Maximal stimulatory effects of bFGF and EGF on eNOS protein expression were observed at 10 ng/ml for 24 h of treatment and were associated with elevated eNOS messenger RNA. PD 98059 also significantly inhibited bFGF- and EGF-induced increases in eNOS protein expression. Because treatment with all three growth factors resulted in activation of the MAPK cascade, while bFGF and EGF, but not VEGF, increased eNOS expression, we conclude that activation of the MAPK cascade is necessary, but not sufficient, for bFGF- and EGF-induced increases in eNOS protein expression in ovine fetoplacental artery endothelial cells. Thus, additional signaling pathways are implicated in the different controls of eNOS expression and mitogenesis by growth factors.

Abstract P038: Dietary Capsaicin May Decrease Blood Pressure Through Enhancing NO With eNOS Activation in 2-Kidney, 1-Clip Hypertensive Rats

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Yukiko Segawa ◽  
Hiroko Hashimoto ◽  
Tomoko Osera ◽  
Nobutaka Kurihara
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Mrna Expression ◽  
Dietary Therapy ◽  
Left Renal Artery ◽  
Sham Operation ◽  
Hypertensive Rats ◽  
Enos Mrna ◽  
Enos Protein Expression ◽  
Enos Protein

Objective: Capsaicin, a component of chili peppers, is reported to have beneficial effects on cardiovascular system through the vasodilative effects. We recently demonstrated the alleviation of blood pressure (BP) elevation by consuming a low concentration of capsaicin diet in 2-kidney, 1-clip (2K1C) hypertensive rats. Since the alleviation was diminished when 2K1C rats took NG-nitro-L-arginine methyl ester, a NO synthase (NOS) inhibitor, during the protocol, we hypothesized that NO has a key role in the effect of capsaicin in 2K1C rats. In this study, we observed eNOS mRNA expression and protein expressions of eNOS and phosphorylated eNOS in 2K1C rats fed a diet containing capsaicin. Methods: Six-week old male Sprague-Dawley rats were treated with sham operation (SHAM) or clipping the left renal artery (2K1C). One week after the surgery, each group of rats were further divided into 2 groups randomly, which received either a control diet (CTL) or a diet containing 0.006% capsaicin (CAP) for 6 weeks. The systolic BP was measured by a tail-cuff method once per week throughout the protocol. At the end of the protocol, rats were euthanized and the abdominal aortas were collected for extracting mRNA and protein. Then, the expression of eNOS mRNA and protein in aorta was evaluated in each group of rats by real time RT-PCR and Western blotting. Results: As shown in Table, capsaicin diet alleviated BP elevation in 2K1C rats. After the dietary protocol, eNOS mRNA expression in 2K1C-CAP was significantly higher than in 2K1C-CTL. Although there were no significant differences in eNOS protein expression among four groups, phosphorylated eNOS protein expression in 2K1C-CAP was marginally significantly higher than in 2K1C-CTL. The expression was also significantly higher in 2K1C rats than in SHAM. Discussion: The present data suggested that dietary capsaicin decreases BP through enhancing NO with activation of eNOS in 2K1C hypertensive rats. It may be a clue for developing a dietary therapy for prevention of hypertension.

NO from smooth muscle cells decreases NOS expression in endothelial cells: role of TNF-α

1999 ◽  
Vol 277 (4) ◽  
pp. H1317-H1325 ◽  
Author(s):  
Trinidad de Frutos ◽  
Lourdes Sánchez de Miguel ◽  
Margarita García-Durán ◽  
Fernando González-Fernández ◽  
Juan A. Rodríguez-Feo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Protein Expression ◽  
Enos Expression ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Enos Protein Expression ◽  
Enos Protein

Despite the evidence that cytokines stimulate nitric oxide (NO) production by inducible nitric oxide synthase (iNOS), several reports recently demonstrated that the hypotensive response related to endothelial nitric oxide synthase (eNOS) activity could be inhibited by the same cytokines. The aim of the present work was to analyze whether NO generated by vascular smooth muscle cells (VSMC) could modify eNOS protein expression in endothelial cells. Bovine aortic endothelial cells (BAEC) and bovine VSMC (BVSMC) in coculture were used for the study. Interleukin-1β (IL-1β, 10 ng/ml)-treated BVSMC, which expressed iNOS protein, decreased eNOS protein expression in BAEC. The presence of NO antagonists N ω-nitro-l-arginine methyl ester (10−3 mol/l) or N G-monomethyl-l-arginine (10−3 mol/l) prevented the decrease in eNOS protein expression induced by IL-1β-treated BVSMC. Surprisingly, two different NO donors, 3-morpholinosydnonimine (10−4 mol/l) and S-nitroso- N-acetyl-d,l-penicillamine (10−4 mol/l), failed to modify eNOS expression in BAEC, suggesting the existence of a diffusible mediator released from IL-1β-treated BVSMC that acts on endothelial cells by reducing eNOS expression. The presence of NO antagonists reduced tumor necrosis factor-α (TNF-α) production by IL-1β-stimulated BVSMC. This effect was also produced in the presence of a protein kinase G inhibitor, guanosine-5′-O-(2-thiodiphosphate) trilithium salt. A polyclonal antibody against TNF-α prevented eNOS expression in the BAEC-BVSMC coculture. In conclusion, NO by itself failed to modify eNOS protein expression in endothelial cells but increased TNF-α generation by IL-1β-stimulated BVSMC and, in this way, reduced eNOS expression in the endothelium.

Oxygen upregulates nitric oxide synthase gene expression in ovine fetal pulmonary artery endothelial cells

1996 ◽  
Vol 270 (4) ◽  
pp. L643-L649 ◽  
Author(s):  
A. J. North ◽  
K. S. Lau ◽  
T. S. Brannon ◽  
L. C. Wu ◽  
L. B. Wells ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Protein Expression ◽  
Oxygen Tension ◽  
Enos Gene ◽  
Enos Expression ◽  
Ovine Fetal ◽  
Enos Protein Expression ◽  
Enos Protein

Nitric oxide (NO) is critically involved in oxygen-mediated pulmonary vasodilatation in the fetus and newborn. We determined the effects of prolonged alterations in oxygenation on endothelial NO synthase (eNOS) gene expression in early passage ovine fetal intrapulmonary artery endothelial cells (PAEC). PAEC were exposed to PO2 = 50 or 150 mmHg for 48 h, and eNOS protein expression was evaluated by immunoblot analysis. eNOS protein expression was 2.7-fold greater at higher oxygen tension; eNOS upregulation was also evident after 24 h. Inducible NOS protein was not detectable by immunoblot at either level of oxygenation. In the lung, the effect of oxygen on eNOS expression may be specific to the endothelium, as eNOS expression in bronchiolar epithelial cells of Clara cell lineage was not altered by varying oxygen tension. The oxygen-related increase in eNOS protein in the fetal PAEC was associated with 2.5-fold greater NOS enzymatic activity. In parallel, there was a 2.8-fold rise in eNOS mRNA abundance. Thus eNOS gene expression in ovine fetal PAEC is upregulated by oxygen, and this is mediated at the level of gene transcription or mRNA stability. This process may play an important role in oxygen modulation of pulmonary vasomotor tone in the fetus and newborn.

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