INT49252

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Context Info
Confidence 0.69
First Reported 1995
Last Reported 2010
Negated 1
Speculated 0
Reported most in Abstract
Documents 17
Total Number 18
Disease Relevance 6.55
Pain Relevance 0.66

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

extracellular space (EDN1) extracellular region (EDN1) cell-cell signaling (EDN1)
cytoplasm (EDN1)
Anatomy Link Frequency
endothelial cells 14
plasma 2
endothelium 2
EDN1 (Homo sapiens)
Pain Link Frequency Relevance Heat
anesthesia 4 89.52 High High
antagonist 113 88.24 High High
cva 44 81.84 Quite High
Inflammation 74 64.00 Quite High
cytokine 48 63.60 Quite High
Catecholamine 2 61.44 Quite High
Kinase C 25 55.32 Quite High
headache 4 44.68 Quite Low
agonist 2 31.52 Quite Low
Analgesic 8 25.00 Low Low
Disease Link Frequency Relevance Heat
Pulmonary Hypertension 130 99.84 Very High Very High Very High
Reprotox - General 1 16 99.76 Very High Very High Very High
Sprains And Strains 8 99.74 Very High Very High Very High
Papillomavirus Infection 4 99.16 Very High Very High Very High
Metastasis 13 96.24 Very High Very High Very High
Osteoporosis 8 95.60 Very High Very High Very High
Hypotension 6 92.12 High High
Hyperinsulinism 16 91.84 High High
Obesity 16 90.92 High High
Hemorrhagic Shock 46 88.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This increase in big ET-1 release appeared to be partly due to a transient stimulation of the expression of prepro ET-1 mRNA.
Positive_regulation (increase) of Localization (release) of ET-1
1) Confidence 0.69 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Phosphoramidon enhanced the big ET-1 release from the cells in a concentration-dependent manner.
Positive_regulation (enhanced) of Localization (release) of ET-1
2) Confidence 0.69 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
When high concentrations of phosphoramidon were added, there was a dramatic increase in the release of big ET-1, which cannot be explained only by the drug-induced inhibition of ECE.
Positive_regulation (increase) of Localization (release) of ET-1
3) Confidence 0.69 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells.
Positive_regulation (induced) of Localization (secretion) of ET-1 in endothelial cells associated with sprains and strains
4) Confidence 0.67 Published 2009 Journal Anesthesiology Section Abstract Doc Link 19104173 Disease Relevance 0.27 Pain Relevance 0.09
CONCLUSIONS: The authors demonstrate for the first time that propofol inhibits strain-induced ET-1 secretion and enhances strain-increased nitric oxide production in human umbilical vein endothelial cells.
Positive_regulation (induced) of Localization (secretion) of ET-1 in endothelial cells
5) Confidence 0.67 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Positive_regulation (generation) of Localization (release) of ET-1 in endothelial cells
6) Confidence 0.50 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Positive_regulation (generation) of Localization (release) of endothelin-1 in endothelial cells
7) Confidence 0.50 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Positive_regulation (generation) of Localization (release) of endothelin-1 in endothelial cells
8) Confidence 0.50 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Positive_regulation (generation) of Localization (release) of ET-1 in endothelial cells
9) Confidence 0.50 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells.
Positive_regulation (induced) of Localization (secretion) of endothelin-1 in endothelial cells associated with sprains and strains
10) Confidence 0.49 Published 2009 Journal Anesthesiology Section Abstract Doc Link 19104173 Disease Relevance 0.27 Pain Relevance 0.09
The former effect appears to be based on the inhibition of ET-1 degradation by neutral endopeptidase 24.11 (NEP), since kelatorphan, a specific NEP inhibitor, produced a similar increasing effect on ET-1 release.
Positive_regulation (increasing) of Localization (release) of ET-1
11) Confidence 0.46 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Furthermore, in the presence of PTIO, a nitric oxide scavenger, and KT5823, a specific inhibitor of cyclic guanosine monophosphate-dependent protein kinase, the inhibitory effect of propofol on strain-induced extracellular signal-regulated protein kinase phosphorylation and ET-1 release was reversed.
Positive_regulation (induced) of Localization (release) of ET-1
12) Confidence 0.45 Published 2009 Journal Anesthesiology Section Body Doc Link 19104173 Disease Relevance 0 Pain Relevance 0
Despite these limitations, studies have established that plasma ET-1 levels are increased in PAH and that pulmonary expression and release of ET-1 is increased in PAH (Stewart et al 1991).
Positive_regulation (increased) of Localization (release) of ET-1 in plasma associated with pulmonary hypertension
13) Confidence 0.36 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761178 Disease Relevance 0.53 Pain Relevance 0.09
Human papillomavirus (HPV)-positive human cervical carcinoma cell lines overexpress ET-1 and ETAR mRNA and secrete ET-1 protein compared to HPV-negative cells.
Positive_regulation (overexpress) of Localization (secrete) of ET-1 associated with papillomavirus infection and reprotox - general 1
14) Confidence 0.25 Published 2004 Journal J Transl Med Section Body Doc Link PMC436068 Disease Relevance 2.32 Pain Relevance 0.13
In theory, selective ETA blockade would prevent the most salient vasoconstrictive and mitogenic effects of ET-1 while maintaining ETB mediated release of NO and prostacyclin and maximal clearance of circulating ET-1 (Vatter and Seifert 2006).
Positive_regulation (mediated) of Localization (release) of ET-1
15) Confidence 0.24 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761178 Disease Relevance 0.57 Pain Relevance 0.08
This probably leads to decreased NO production and increased ET-1 secretion, characteristic of endothelial dysfunction.
Neg (NO) Positive_regulation (increased) of Localization (secretion) of ET-1
16) Confidence 0.19 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2903979 Disease Relevance 1.19 Pain Relevance 0.11
When angiotensin II binds the angiotensin II type 1 receptor on endothelial cells, it stimulates the production of ROS via NADPH oxidase, increases expression of ICAM-1 and increases ET-1 release from the endothelium [52–54].
Positive_regulation (increases) of Localization (release) of ET-1 in endothelium
17) Confidence 0.19 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2903979 Disease Relevance 0.94 Pain Relevance 0.03
The clinical impact is not yet fully understood, but possible underlying mechanisms include scavenging of nitric oxide, augmented release of endothelin, and stimulation of endothelin receptors and adrenoreceptors [117-120].
Positive_regulation (augmented) of Localization (release) of endothelin
18) Confidence 0.01 Published 2008 Journal Crit Care Section Body Doc Link PMC2575549 Disease Relevance 0.45 Pain Relevance 0.04

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