INT156097

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.58
First Reported 2003
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 70
Total Number 71
Disease Relevance 34.96
Pain Relevance 4.17

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 (VEGFA) growth (VEGFA) extracellular region (VEGFA)
proteinaceous extracellular matrix (VEGFA) cytoplasm (VEGFA)
Anatomy Link Frequency
endothelial cells 12
chondrocyte 6
NK cells 6
liver 4
HT-1080 4
VEGFA (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 873 100.00 Very High Very High Very High
antagonist 69 99.98 Very High Very High Very High
metalloproteinase 1073 99.80 Very High Very High Very High
COX-2 inhibitor 222 99.12 Very High Very High Very High
fluoxetine 6 98.60 Very High Very High Very High
positron emission tomography 114 96.36 Very High Very High Very High
Inflammation 594 96.28 Very High Very High Very High
Eae 1 92.64 High High
agonist 70 91.92 High High
antidepressant 6 89.44 High High
Disease Link Frequency Relevance Heat
Infection 956 99.98 Very High Very High Very High
Glioblastoma 5 99.84 Very High Very High Very High
Cancer 2605 99.80 Very High Very High Very High
Herpes Simplex Virus 2142 99.78 Very High Very High Very High
Pancreatic Cancer 126 99.62 Very High Very High Very High
Squamous Cell Carcinoma 45 99.54 Very High Very High Very High
Sarcoma 724 99.52 Very High Very High Very High
Fibrosarcoma 29 99.36 Very High Very High Very High
Apoptosis 307 99.20 Very High Very High Very High
Uterine Cancer 1 99.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The inhibitory effect of clonidine on the secretion of VEGF protein stimulated with IL-1beta was blocked by alpha(2)-ADR antagonists.
Negative_regulation (effect) of Localization (secretion) of VEGF protein
1) Confidence 0.58 Published 2009 Journal Graefes Arch. Clin. Exp. Ophthalmol. Section Body Doc Link 19011889 Disease Relevance 0 Pain Relevance 0
Inhibition of mTOR reduces secretion of VEGF by the tumor through inhibition of HIF-1?.
Negative_regulation (reduces) of Localization (secretion) of VEGF associated with cancer
2) Confidence 0.47 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2804796 Disease Relevance 1.36 Pain Relevance 0.14
The inhibitory effect of clonidine on the secretion of VEGF protein stimulated with IL-1beta was blocked by alpha(2)-ADR antagonists.
Negative_regulation (blocked) of Localization (secretion) of VEGF protein
3) Confidence 0.43 Published 2009 Journal Graefes Arch. Clin. Exp. Ophthalmol. Section Body Doc Link 19011889 Disease Relevance 0 Pain Relevance 0
At the control secretion rates of VEGF and sVEGFR1 needed to reproduce these selected plasma concentrations, our predicted interstitial concentrations ([V]IS?
Negative_regulation (rates) of Localization (secretion) of VEGF in plasma
4) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Hence in seeking our control sVEGFR1-secretion rates, we redefined the control VEGF-secretion rates to qV,+Ctrl?
Negative_regulation (redefined) of Localization (secretion) of VEGF-secretion
5) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Similarly, we also showed that PO reduced the expression of PI3K, subsequently downregulated the phosphorylation of AKT, and VEGF secretion in HT-1080 sarcoma cells.
Negative_regulation (downregulated) of Localization (secretion) of VEGF in HT-1080 associated with sarcoma
6) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925949 Disease Relevance 0.24 Pain Relevance 0
We also showed that PO suppressed PI3K/AKT signaling and reduced VEGF secretion and expression fibrosarcoma HT-1080 cells, which is consistent with the current understanding of the role of VEGF/PI3K in angiogenesis.
Negative_regulation (reduced) of Localization (secretion) of VEGF in HT-1080 associated with fibrosarcoma
7) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925949 Disease Relevance 0.41 Pain Relevance 0
We also show that activation of 5-HT1A receptors is sufficient to induce VEGF expression and that a 5-HT1A antagonist blocks both the increase in VEGF and behavioral effects induced by fluoxetine.
Negative_regulation (blocks) of Localization (increase) of VEGF associated with antagonist and fluoxetine
8) Confidence 0.37 Published 2009 Journal Neuropsychopharmacology Section Abstract Doc Link 19553916 Disease Relevance 0.15 Pain Relevance 0.94
Although calcium and thrombin induce immediate growth factor release from platelet in a dose-dependent manner,24 high concentrations of thrombin could present an adverse effect on migration and proliferation of vascular endothelial cells.14,15 Also thrombin has a threshold effect in relation to VEGF release, and high concentrations of thrombin decrease the release of VEGF.25 Because the exact threshold mechanism and concentration of thrombin are unknown, we set the concentration of thrombin and calcium optimal for vascular endothelial cell proliferation.
Negative_regulation (decrease) of Localization (release) of VEGF in endothelial cells
9) Confidence 0.34 Published 2010 Journal The Journal of Advanced Prosthodontics Section Body Doc Link PMC2984511 Disease Relevance 0 Pain Relevance 0
CONCLUSION

Alendronate, a nitrogen containing bisphosphonate, reduced secreted VEGF at the mRNA, protein, and secretory levels in growth plate chondrocytes indicating that bisphosphonates inhibit cellular turnover at the chondro-osseous junction by reducing VEGF induced vascular invasion.

Negative_regulation (reduced) of Localization (secreted) of VEGF in growth plate
10) Confidence 0.32 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.23 Pain Relevance 0
A preferential decrease in the secreted VEGF forms by alendronate corresponds to the reduced vascular invasion at the chondro-osseous junction as seen in vivo following treatment with another bisphosphonate, pamidronate [30].
Negative_regulation (decrease) of Localization (secreted) of VEGF
11) Confidence 0.32 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.05 Pain Relevance 0
These data would suggest that alendronate altered the cellular content of both farnesylated and geranylgeranylated proteins important in the secretory process which in turn impaired release of the VEGF protein from the cell.
Negative_regulation (impaired) of Localization (release) of VEGF
12) Confidence 0.32 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.18 Pain Relevance 0
By blocking isoprenoid modification, the alendronate may have further reduced the capacity of the chondrocyte to secrete VEGF beyond a reduction in transcription of the secreted form(s).
Negative_regulation (reduced) of Localization (secrete) of VEGF in chondrocyte
13) Confidence 0.32 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.20 Pain Relevance 0
Blocking secreted VEGF and inhibiting osteoclast function by reducing geranylgeranylated proteins by alendronate is consistent with the impaired vascular invasion and the reduced osteoclastic activity seen with bisphosphonates in vivo [30].
Negative_regulation (Blocking) of Localization (secreted) of VEGF in osteoclast associated with osteoporosis
14) Confidence 0.32 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.16 Pain Relevance 0
Low alendronate treatment alone and when combined with mevalonate pathway intermediates significantly reduced VEGF protein secreted into the media accompanied by an increase in cell associated VEGF.
Negative_regulation (reduced) of Localization (secreted) of VEGF
15) Confidence 0.32 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.07 Pain Relevance 0
Reperfusion is because bevacizumab blocks the VEGF already secreted in the vitreous cavity but further secretion from the ischemic retina will continue.
Negative_regulation (blocks) of Localization (secreted) of VEGF in cavity
16) Confidence 0.28 Published 2007 Journal Clinical ophthalmology (Auckland, N.Z.) Section Body Doc Link PMC2704517 Disease Relevance 0.40 Pain Relevance 0.06
The incomplete inhibition of VEGF secretion by COX-2 chemical inhibitors suggested that besides COX-2, other factors induced by KSHV infection might also be playing a role in VEGF release from infected cells.


Negative_regulation (inhibition) of Localization (secretion) of VEGF associated with herpes simplex virus and infection
17) Confidence 0.25 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.50 Pain Relevance 0
COX-2 silencing also inhibited VEGF-A and VEGF-C secretion but to a lesser extent than chemical inhibitor treatment (Figures 6B-6E).
Negative_regulation (inhibited) of Localization (secretion) of VEGF
18) Confidence 0.25 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.60 Pain Relevance 0
Analyses showed that NS-398 pretreatment inhibited VEGF-A and VEGF-C secretion which was higher than inhibition by Indo treatment (Figures 6B and 6D).
Negative_regulation (inhibited) of Localization (secretion) of VEGF
19) Confidence 0.25 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.61 Pain Relevance 0
Treatment of cells with either NS-398 or Indo prior to KSHV infection reduced VEGF-A and VEGF-C secretion at all the time points tested (Figures 6B and 6D).
Negative_regulation (reduced) of Localization (secretion) of VEGF associated with herpes simplex virus and infection
20) Confidence 0.25 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.62 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox