INT249873

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Context Info
Confidence 0.53
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 19
Disease Relevance 7.33
Pain Relevance 2.71

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

signal transduction (Gpr17) plasma membrane (Gpr17) signal transducer activity (Gpr17)
Anatomy Link Frequency
neurons 3
brain 2
cortex 2
oligodendrocyte 2
macrophages 1
Gpr17 (Mus musculus)
Pain Link Frequency Relevance Heat
ischemia 304 99.96 Very High Very High Very High
agonist 247 99.24 Very High Very High Very High
antagonist 152 98.86 Very High Very High Very High
Hippocampus 57 90.00 High High
excitatory amino acid 19 74.96 Quite High
Central nervous system 38 48.56 Quite Low
Inflammation 76 45.08 Quite Low
Spinal cord 19 44.00 Quite Low
Multiple sclerosis 57 40.48 Quite Low
Inflammatory response 19 39.48 Quite Low
Disease Link Frequency Relevance Heat
Middle Cerebral Artery Infarction 551 99.96 Very High Very High Very High
Cv Unclassified Under Development 209 99.96 Very High Very High Very High
Brain Hemorrhage 152 99.96 Very High Very High Very High
Injury 133 99.96 Very High Very High Very High
Brain Injury 171 99.76 Very High Very High Very High
Stress 38 94.84 High High
Death 228 83.88 Quite High
Cv General 4 Under Development 19 74.72 Quite High
Demyelinating Disease 114 72.96 Quite High
Targeted Disruption 57 55.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Upon brain ischemia, GPR17 is induced in several embryonically different cells that participate to damage evolution and repair
Positive_regulation (induced) of GPR17 in brain associated with brain hemorrhage and ischemia
1) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.43 Pain Relevance 0.26
Globally, these data show that induction of brain damage is associated to activation of GPR17.
Positive_regulation (activation) of GPR17 in brain
2) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.42 Pain Relevance 0.04
LTD4, which also acts as an agonist at GPR17 ([11]; the present study), induced similar effects, suggesting that activation of GPR17 on oligodendrocyte precursors by its endogenous agonists promotes progression along their differentiation pathway.
Positive_regulation (activation) of GPR17 in oligodendrocyte associated with agonist
3) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0 Pain Relevance 0.35
In treated cultures, the total number of cells was not increased, to suggest that activation of GPR17 is actually inducing the maturation of already existing precursors.
Positive_regulation (activation) of GPR17
4) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.05 Pain Relevance 0.38
Moreover, in the MCAo rat model, 48 hours after ischemia induction, GPR17-immunoreactivity was markedly increased in the ipsilateral cortex both within and at the borders of the ischemic infarct, suggesting a potential role in the evolution of ischemic damage.
Positive_regulation (increased) of GPR17-immunoreactivity in cortex associated with middle cerebral artery infarction and ischemia
5) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.37 Pain Relevance 0.12
The total number of cells in culture did not significantly increase during the 72 h treatment period with pharmacological agents, as suggested by labeling of cell nuclei with Hoechst 33258 (Figure 4L and 4M), to support the conclusion that, in these cultures, activation of GPR17 by its endogenous agonists is actually inducing the in vitro maturation of already existing oligodendrocyte precursors.
Positive_regulation (activation) of GPR17 in oligodendrocyte associated with agonist
6) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.25 Pain Relevance 0.13
Very early (24 h) after the insult, GPR17 is transiently upregulated in neurons (which already express this receptor under physiological conditions) in parallel with the appearance of the cellular stress marker HSP70.
Positive_regulation (upregulated) of GPR17 in neurons associated with stress
7) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.49 Pain Relevance 0.04
Consistent with this hybrid pharmacology, activation of GPR17 by uracil nucleotides was counteracted by the P2Y receptor antagonists cangrelor and MRS2179, whereas its activation by cysLTs was antagonized by montelukast and pranlukast, two already marketed CysLT receptor blockers (ibidem).
Positive_regulation (activation) of GPR17 associated with antagonist
8) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.56 Pain Relevance 0.12
These data show that after up-regulation in neurons, there is a second wave of GPR17 induction in microglia/macrophages as soon as these cells are activated and recruited toward the lesioned area as a consequence of damage.
Positive_regulation (induction) of GPR17 in neurons
9) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.40 Pain Relevance 0
Several of these cells were also immunoreactive for GPR17 (red fluorescence in Figure 3A; cells expressing both S100?
Positive_regulation (fluorescence) of GPR17
10) Confidence 0.39 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.06 Pain Relevance 0.08
Exposure to a maximal concentration (100 nM) of LTD4 also significantly increased both the number of GPR17+ and mature MBP+ oligodendroglial cells (Figure 4M).
Positive_regulation (increased) of GPR17
11) Confidence 0.39 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.08 Pain Relevance 0.08
Following ischemia, GPR17 is sequentially induced in neurons, microglia/macrophages and adult oligodendrocyte precursor cells, suggesting that it may act as a common regulatory gene mediating response to injury in embryonically-distinct cell types.
Positive_regulation (induced) of GPR17 in macrophages associated with ischemia and injury
12) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.85 Pain Relevance 0.16
These apparently conflicting results suggest that GPR17 might play differential roles in different cell types and/or under specific pathophysiological conditions; for example, it may well be that, upon injury, GPR17 is induced in distinct cell types depending upon specific phases of damage development, remodeling and repair.
Positive_regulation (induced) of GPR17 associated with injury
13) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.43 Pain Relevance 0.03
In summary, our study reveals the new cysLT/uracil nucleotide receptor GPR17 as a “sensor” that is activated upon brain injury in several embryonically distinct cell types (neurons, microglia and adult neural precursor cells) that contribute to damage evolution and to the subsequent remodeling and repair.
Positive_regulation (activated) of GPR17 in precursor cells associated with brain injury
14) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.43 Pain Relevance 0.20
Within the lesioned area, a strong up-regulation of GPR17 was observed 24 h after MCAo (Figure 5A) with respect to the corresponding unlesioned area of the contralateral cortex (Figure 5C).
Positive_regulation (regulation) of GPR17 in cortex associated with middle cerebral artery infarction
15) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.42 Pain Relevance 0.11
One week after MCAo, GPR17 immunopositivity was again increased within the damaged area: also these cells were all IB4+, suggesting that they are indeed the macrophages/microglia found at the lesion borders at day 3, that were now infiltrating the lesioned area (data not shown).
Positive_regulation (increased) of GPR17 in IB4 associated with middle cerebral artery infarction
16) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.38 Pain Relevance 0
To confirm the specificity of these effects, we demonstrated that the P2Y receptor antagonist cangrelor (that was previously demonstrated to contrast GPR17 activation both in vitro and in vivo [11], the present study), partially counteracted UDP-glucose induced changes.
Positive_regulation (activation) of GPR17 associated with antagonist
17) Confidence 0.36 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0 Pain Relevance 0.29
Following ischemia, GPR17 is sequentially induced in neurons, microglia/macrophages and adult oligodendrocyte precursor cells, suggesting that it may act as a common regulatory gene mediating response to injury in embryonically-distinct cell types.
Positive_regulation (induced) of GPR17 in microglia associated with ischemia and injury
18) Confidence 0.12 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.85 Pain Relevance 0.16
Following ischemia, GPR17 is sequentially induced in neurons, microglia/macrophages and adult oligodendrocyte precursor cells, suggesting that it may act as a common regulatory gene mediating response to injury in embryonically-distinct cell types.
Positive_regulation (induced) of GPR17 in neurons associated with ischemia and injury
19) Confidence 0.12 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570486 Disease Relevance 0.85 Pain Relevance 0.16

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