INT123927

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Context Info
Confidence 0.48
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 10.18
Pain Relevance 0.71

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

cell differentiation (Angpt1) signal transduction (Angpt1) extracellular space (Angpt1)
extracellular region (Angpt1) plasma membrane (Angpt1) molecular_function (Angpt1)
Anatomy Link Frequency
bone marrow 4
myocardium 2
vessels 2
artery smooth muscle 2
heart 2
Angpt1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
fibrosis 136 97.60 Very High Very High Very High
ischemia 37 90.12 High High
Central nervous system 1 85.92 High High
Angina 10 82.72 Quite High
metalloproteinase 1 81.08 Quite High
Inflammation 15 70.96 Quite High
cytokine 24 69.92 Quite High
chemokine 1 65.00 Quite High
Serotonin 7 55.44 Quite High
Neuronal nitric oxide synthase 1 42.96 Quite Low
Disease Link Frequency Relevance Heat
Myocardial Infarction 627 99.74 Very High Very High Very High
Diabetes Mellitus 837 99.68 Very High Very High Very High
Pulmonary Hypertension 158 99.54 Very High Very High Very High
Fibrosis 145 98.32 Very High Very High Very High
Ventricular Remodeling 90 96.92 Very High Very High Very High
Apoptosis 32 91.16 High High
Coronary Artery Disease 45 90.12 High High
Stress 20 89.36 High High
Infarction 13 89.24 High High
Congenital Anomalies 2 84.64 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In our present study, the strategy of combination gene therapy markedly increased the expression of VEGF and Ang-1 in the diabetic ischemic heart compared with the Ad.LacZ-treated diabetic MI group.
Positive_regulation (increased) of Gene_expression (expression) of Ang-1 in heart associated with diabetes mellitus and myocardial infarction
1) Confidence 0.48 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 1.15 Pain Relevance 0.05
A strategy to locally overexpress VEGF and Ang-1 in combination would prove beneficial because, although VEGF can take the lead in the process of neovascularization, Ang-1 would be expected to support the maturation of the newly formed vessels.
Positive_regulation (overexpress) of Gene_expression (overexpress) of Ang-1 in vessels
2) Confidence 0.48 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 0.83 Pain Relevance 0.06
Similarly, we observed a significant increase in the expression of Ang-1 (4.0-fold) and Tie-2 (2.1-fold) in the diabetic animals that received the therapy (DVAMI), 4 days after the treatment, compared with the Ad.LacZ-treated diabetic MI (DLZMI) group (Fig. 4C and D).


Positive_regulation (increase) of Gene_expression (expression) of Ang-1 associated with diabetes mellitus and myocardial infarction
3) Confidence 0.48 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 1.00 Pain Relevance 0
Our treatment strategy leading to the coexpression of VEGF and Ang-1 might have led to the increased expression of survivin through the activation of NF?
Positive_regulation (leading) of Gene_expression (coexpression) of Ang-1
4) Confidence 0.35 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 0.82 Pain Relevance 0.10
Immediately after MI, adenoviral vectors encoding for VEGF (Ad.VEGF, 6 × 107 pfu) and Ang-1 (Ad.Ang1, 1.5 × 105 pfu) were intramyocardially administered in combination (in 100 ?
Positive_regulation (vectors) of Gene_expression (encoding) of Ang-1 associated with myocardial infarction
5) Confidence 0.35 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 0.72 Pain Relevance 0
Moreover, there is evidence that suggests that post-MI vascular repair is not dependent solely on the activation and participation of resident endothelial cells, but may also reflect an increased bone marrow–derived endothelial progenitor cell mobilization and homing, which are in turn activated by overexpression of both VEGF and Ang-1 (43,44).
Positive_regulation (activated) of Gene_expression (overexpression) of Ang-1 in bone marrow associated with myocardial infarction
6) Confidence 0.35 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 0.84 Pain Relevance 0.03
Moreover, there is evidence that suggests that post-MI vascular repair is not dependent solely on the activation and participation of resident endothelial cells, but may also reflect an increased bone marrow–derived endothelial progenitor cell mobilization and homing, which are in turn activated by overexpression of both VEGF and Ang-1 (43,44).
Positive_regulation (overexpression) of Gene_expression (overexpression) of Ang-1 in bone marrow associated with myocardial infarction
7) Confidence 0.35 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 0.84 Pain Relevance 0.03
The therapy significantly reduced the ventricular remodeling as evidenced by the significant reduction in the collagenous fibrotic tissue and improvement in the myocardial functions in conjunction with significant increase in the levels of VEGF and its receptor Flk-1, Ang-1 and its receptor Tie-2, p-MK2, and antiapoptotic survivin.
Positive_regulation (increase) of Gene_expression (levels) of Ang-1 associated with fibrosis and ventricular remodeling
8) Confidence 0.32 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 1.15 Pain Relevance 0.03
Similarly, the expression of VEGF and Ang-1 was restored markedly upon treatment in the diabetic (DVAMI) myocardium (Fig. 1B and C).


Positive_regulation (restored) of Gene_expression (expression) of Ang-1 in myocardium associated with diabetes mellitus
9) Confidence 0.32 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 0.79 Pain Relevance 0.11
Cell-based gene transfer with angiopoietin-1 (Ang-1), a newly discovered ligand of the endothelial-specific tyrosine kinase receptor Tie-2, has been shown to improve survival and pulmonary hemodynamics in experimental PAH by a mechanism involving the inhibition of apoptosis and protection of the pulmonary microvasculature [58].

2.2.5.

Positive_regulation (transfer) of Gene_expression (transfer) of angiopoietin-1 associated with pulmonary hypertension and apoptosis
10) Confidence 0.30 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2843902 Disease Relevance 0.89 Pain Relevance 0.10
In the present study, prior treatment of cells with cyclopamine and chel abrogated the expression of iNOS and angiogenic growth factors including VEGF, Ang-1 and netrin-1 thus suggesting that these pro-angiogenesis relevant molecular events were PKC dependent.
Positive_regulation (abrogated) of Gene_expression (expression) of Ang-1
11) Confidence 0.14 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.06 Pain Relevance 0.08
Severe pulmonary hypertension is associated with an increased expression of the angiogenic factor, angiopoietin-1, which shuts off the expression of BMPR1A, a transmembrane protein necessary for BMPR2 signalling, and thereby causes pulmonary artery smooth muscle cell proliferation.
Positive_regulation (increased) of Gene_expression (expression) of angiopoietin-1 in artery smooth muscle associated with pulmonary hypertension
12) Confidence 0.01 Published 2004 Journal Bull. Mem. Acad. R. Med. Belg. Section Abstract Doc Link 15615096 Disease Relevance 1.09 Pain Relevance 0.11

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