INT253191

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.66
First Reported 2008
Last Reported 2010
Negated 3
Speculated 0
Reported most in Body
Documents 2
Total Number 29
Disease Relevance 2.57
Pain Relevance 1.14

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

anatomical structure formation involved in morphogenesis (Shh) Golgi apparatus (Shh) endoplasmic reticulum (Shh)
embryo development (Shh) cell-cell signaling (Shh) signal transducer activity (Shh)
Anatomy Link Frequency
MSCs 6
heart 6
bone marrow 4
myocardium 2
cardiomyocytes 2
Shh (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cytokine 85 97.96 Very High Very High Very High
Inflammation 30 97.60 Very High Very High Very High
fibrosis 28 93.60 High High
ischemia 28 88.44 High High
Neuronal nitric oxide synthase 28 87.60 High High
anesthesia 29 87.32 High High
Central nervous system 28 61.68 Quite High
Kinase C 2 34.00 Quite Low
metalloproteinase 28 31.48 Quite Low
Inflammatory response 28 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 58 97.60 Very High Very High Very High
Apoptosis 38 96.48 Very High Very High Very High
Diabetes Mellitus 50 96.20 Very High Very High Very High
Injury 56 94.92 High High
Fibrosis 28 93.60 High High
Cancer 30 90.24 High High
Cv Unclassified Under Development 28 88.44 High High
Myocardial Infarction 168 78.64 Quite High
Increased Venous Pressure Under Development 28 75.92 Quite High
Gestational Diabetes 9 67.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition to upregulation of Ptc1, overexpression of Shh in MSCs stimulated the expression of secretable angiogenic growth factors including Ang-1 and VEGF.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh
1) Confidence 0.66 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0.06
We also found that Shh overexpression also induced panPKC fragment PKM (45 kd; a proteolytic subunit of PKC) in ShhMSCs which was completely abolished by pretreatment of the cells with 2.5 µM chel or 1 µM cyclopamine (Figure 3E).
Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh
2) Confidence 0.66 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0
In the present study we took advantage of the anti-apoptotic and pro-angiogenic role of Shh signaling and combined Shh transgene delivery to the infarcted heart by transplantation of mesenchymal stem cells (MSCs) which were non-virally transfected to overexpress Shh.
Positive_regulation (transfected) of Gene_expression (overexpress) of Shh in heart associated with apoptosis
3) Confidence 0.66 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.10 Pain Relevance 0
Our results were in harmony with these data and further showed uniquely that Shh gene overexpression up-regulated iNOS, netrin-1 and HGF in addition to the already reported cytokines.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh gene in HGF associated with cytokine
4) Confidence 0.66 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.15 Pain Relevance 0.20
Measurement of NO activity by using a colorimetric NO assay kit showed that Shh overexpression was associated with a concomitant increase in NO production in ShhMSCs (Figure 3C).
Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh
5) Confidence 0.66 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0
However, since isolated neural stem cells exposed to glucose in vitro show increased gene expression of both Shh and Bmp-4 (50), the exact relationship(s) between gene expression changes in the surrounding tissues and the neural crest cells themselves caused by exposure to a diabetic environment will have be subject to further studies.
Positive_regulation (increased) of Gene_expression (expression) of Shh in neural associated with diabetes mellitus
6) Confidence 0.65 Published 2008 Journal Diabetes Section Body Doc Link PMC2584142 Disease Relevance 0.48 Pain Relevance 0
During Western blot studies, subsequent Shh transfection of the respective siRNA transfected cells showed that PI3K/Akt abrogation failed to block Shh induced iNOS expression (Figure 3D; lane-3).
Positive_regulation (induced) of Gene_expression (expression) of Shh
7) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0
The anticipated objective of our multipronged strategy was to achieve intracrine, autocrine, and paracrine effects of Shh protein which was secreted from MSCs overexpressing Shh (ShhMSCs) and regenerated the damaged tissue, induced revascularization and concomitantly prevented remodeling of the heart by preserving the existing myocardium.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of ShhMSCs in MSCs
8) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.09 Pain Relevance 0
Activation of Shh pathway upregulates the expression of multiple angiogenic cytokines, including VEGF, angiopoietins, SDF-1?
Positive_regulation (Activation) of Gene_expression (pathway) of Shh associated with cytokine
9) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.09 Pain Relevance 0.13
Another interesting finding in the present study was the presence of PKM fragment of PKC in ShhMSCs at 72-h after transfection with Shh plasmid.
Positive_regulation (transfection) of Gene_expression (transfection) of Shh plasmid
10) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.08 Pain Relevance 0.03
The anticipated objective of our multipronged strategy was to achieve intracrine, autocrine, and paracrine effects of Shh protein which was secreted from MSCs overexpressing Shh (ShhMSCs) and regenerated the damaged tissue, induced revascularization and concomitantly prevented remodeling of the heart by preserving the existing myocardium.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of Shh in MSCs
11) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.09 Pain Relevance 0
An outside intervention to overexpress Shh in the heart activated its downstream signaling cascade and strongly induced Patched1 (Ptc1) expression in the cardiomyocytes which indicated an active participation of Shh in the myocardial repair process.
Positive_regulation (activated) of in cardiomyocytes Gene_expression (overexpress) of Shh in heart
12) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.26 Pain Relevance 0.04
These molecular changes were mediated by iNOS/netrin/PKC signaling pathway downstream of Shh gene overexpression which combined with stem cell transplantation could be a promising strategy for the treatment of an infarcted heart.


Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh gene in stem cell
13) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0.05
An outside intervention to overexpress Shh in the heart activated its downstream signaling cascade and strongly induced Patched1 (Ptc1) expression in the cardiomyocytes which indicated an active participation of Shh in the myocardial repair process.
Positive_regulation (overexpress) of Gene_expression (overexpress) of Shh in heart
14) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.26 Pain Relevance 0.04
On the contrary, treatment of MSCs with 2.5 µM chel or 1 µM cyclopamine prior to Shh transfection significantly abolished iNOS expression in ShhMSCs (Figure 3D).
Positive_regulation (transfection) of Gene_expression (transfection) of Shh
15) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0
We also found that Shh overexpression also induced panPKC fragment PKM (45 kd; a proteolytic subunit of PKC) in ShhMSCs which was completely abolished by pretreatment of the cells with 2.5 µM chel or 1 µM cyclopamine (Figure 3E).
Positive_regulation (induced) of Gene_expression (overexpression) of Shh
16) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0
An outside intervention to overexpress Shh in the heart activated its downstream signaling cascade and strongly induced Patched1 (Ptc1) expression in the cardiomyocytes which indicated an active participation of Shh in the myocardial repair process.
Positive_regulation (induced) of in cardiomyocytes Gene_expression (overexpress) of Shh in heart
17) Confidence 0.48 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.26 Pain Relevance 0.04
In one of the experimental studies, more than 15-fold increase in Shh mRNA expression was observed in the ischemic myocardium [6].
Positive_regulation (increase) of Gene_expression (expression) of Shh mRNA in myocardium
18) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.27 Pain Relevance 0.04
Flow cytometry showed that Shh overexpression did not alter surface marker expression in ShhMSCs (Figure S1C).


Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh
19) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0.07
Treatment of the cells with Shh or instrinsic Shh gene overexpression in response to various factors involve signaling pathways including PI3K/Akt, Ras/ERK and PKC.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Shh gene
20) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.08 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox