INT116428

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Context Info
Confidence 0.76
First Reported 2004
Last Reported 2010
Negated 1
Speculated 2
Reported most in Body
Documents 68
Total Number 72
Disease Relevance 35.81
Pain Relevance 7.07

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

transport (Cybb) mitochondrion (Cybb) oxidoreductase activity (Cybb)
Golgi apparatus (Cybb) endoplasmic reticulum (Cybb) plasma membrane (Cybb)
Anatomy Link Frequency
brain 13
microglial cell 9
neurons 6
neuronal 4
synapse 3
Cybb (Mus musculus)
Pain Link Frequency Relevance Heat
chemokine 23 100.00 Very High Very High Very High
Stimulus evoked pain 3 99.92 Very High Very High Very High
Thermal hyperalgesia 6 99.40 Very High Very High Very High
Dorsal horn 3 99.36 Very High Very High Very High
allodynia 6 98.90 Very High Very High Very High
Central nervous system 50 98.42 Very High Very High Very High
cva 68 98.40 Very High Very High Very High
interneuron 185 98.24 Very High Very High Very High
Spinal cord 12 98.12 Very High Very High Very High
GABAergic 333 97.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Aging 852 100.00 Very High Very High Very High
Cancer 81 100.00 Very High Very High Very High
Neutrophil Disorders 65 100.00 Very High Very High Very High
Necrosis 8 100.00 Very High Very High Very High
Hypersensitivity 4 99.92 Very High Very High Very High
Brain Injury 1166 99.72 Very High Very High Very High
Contusions 110 99.60 Very High Very High Very High
Hyperalgesia 6 99.40 Very High Very High Very High
Apoptosis 476 99.38 Very High Very High Very High
Pain 3 99.24 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To identify the cell types expressing gp91phox in the peri-contusional area, cells were co-labelled with antibodies raised against gp91phox and markers of microglial (CD11b), astroglial (GFAP), and neuronal (NeuN) cells (Fig 2B).
Gene_expression (expressing) of gp91phox in neuronal
1) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.95 Pain Relevance 0
Gp91phox is mainly expressed by cytotoxic-type classically activated microglia in the peri-contusional regions after TBI
Gene_expression (expressed) of Gp91phox in microglia associated with brain injury
2) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.89 Pain Relevance 0
In the present study, we demonstrated that gp91phox is mainly expressed in microglia, and at lower levels in neurons and astrocytes.
Gene_expression (expressed) of gp91phox in neurons
3) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.76 Pain Relevance 0
We then tried to identify the microglia that expressed gp91phox by using the mouse microglial cell line BV-2 and by activating these cells with IFN?
Gene_expression (expressed) of gp91phox in microglial cell
4) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.15 Pain Relevance 0
Some recent studies have demonstrated that expression of gp91phox increases in brain after intracerebral hemorrhage, resulting in enhanced lipid peroxidation [24,41].
Gene_expression (expression) of gp91phox in brain associated with cv general 4 under development and cva
5) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.86 Pain Relevance 0.23
Gp91phox is expressed constitutively in neurons but not in glial cells, and O2- production might play a role in neuronal homeostasis [22].
Neg (not) Gene_expression (expressed) of Gp91phox in neurons
6) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.70 Pain Relevance 0
We then demonstrated that the microglial phenotypes expressed both gp91phox and p22phox, which probably reflects the induction of NADPH oxidase in the BV-2 mouse microglial cell line that we used.
Gene_expression (expressed) of gp91phox in microglial cell
7) Confidence 0.76 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.89 Pain Relevance 0
Consistent with a direct effect of IL-6 on Nox2 expression, direct systemic injection of IL-6 into mice increased Nox2 protein and activity, confirming the ability of peripheral IL-6 to mediate increased Nox2 expression and superoxide production in brain.
Gene_expression (expression) of Nox2 in brain
8) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.20 Pain Relevance 0.05
To quantify the age-related increase in Nox2 expression, and assess whether IL-6 was involved in this process, we determined levels of Nox2 protein in young and old wild-type (C57BL/6) and IL-6-deficient (IL-6-/-) animals.
Gene_expression (expression) of Nox2
9) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.12 Pain Relevance 0.04
Previous studies have reported that Nox2 and Nox4 are the only NADPH oxidase isoforms expressed in the adult mouse nervous system[28], a finding we confirmed by RT-PCR in brain of old mice as well (Dugan and Zheng, unpublished).
Gene_expression (expressed) of Nox2 in brain
10) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0 Pain Relevance 0
Consistent with a direct effect of IL-6 on Nox2 expression, direct systemic injection of IL-6 into mice increased Nox2 protein and activity, confirming the ability of peripheral IL-6 to mediate increased Nox2 expression and superoxide production in brain.
Gene_expression (expression) of Nox2 in brain
11) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.12 Pain Relevance 0.04
Moreover, we recently demonstrated that IL-6 can directly induce and activate Nox2 protein expression in cultured neurons[15], but in that study in young mice, acute peripheral injection of IL-6 failed to induce brain Nox2 expression.
Gene_expression (expression) of Nox2 protein in brain
12) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.23 Pain Relevance 0.03
In the context of chronically elevated peripheral IL-6 in aged animals, on the other hand, we wished to determine whether aging was associated with an increase in Nox2 expression in brain, by analyzing Nox2 protein expression in young (4 month old) and old (24 month old) mouse brain.
Gene_expression (expression) of Nox2 protein in brain associated with aging
13) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.18 Pain Relevance 0.04
There were rare GFAP-positive astrocytes which also expressed Nox2.
Gene_expression (expressed) of Nox2 in astrocytes
14) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.15 Pain Relevance 0.05
The robust induction of Nox2 expression and activity we observed led us to ask whether PV inhibitory interneurons might also be selectively lost during aging, as well.
Gene_expression (expression) of Nox2 in inhibitory interneurons associated with aging
15) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.26 Pain Relevance 0.26
Thus, more than 95% or all Nox2-expressing cells in aged mice were Map2-postive neurons.
Gene_expression (expressing) of Nox2 in neurons
16) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.14 Pain Relevance 0.04
IL-6-/- mice lack the age-related increase in Nox2 expression and superoxide production observed in old wild-type mice.
Gene_expression (expression) of Nox2
17) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.05 Pain Relevance 0.03
Nox2 was also found to be constitutively active in synaptosomes; Nox2-dependent O2 consumption and superoxide production in synaptosomes was detected immediately after addition of the substrate, NADPH, and in contrast to a number of other studies which have required agents, such as phorbol esters, to induce assembly of the Nox2 complex, required no other additions to observe O2 consumption and superoxide generation.
Gene_expression (production) of Nox2
18) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0 Pain Relevance 0.03
In the context of chronically elevated peripheral IL-6 in aged animals, on the other hand, we wished to determine whether aging was associated with an increase in Nox2 expression in brain, by analyzing Nox2 protein expression in young (4 month old) and old (24 month old) mouse brain.
Gene_expression (expression) of Nox2 in brain associated with aging
19) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.18 Pain Relevance 0.04
Increased Nox2 protein expression in brain of aged animals is attenuated in IL-6-/- mice
Gene_expression (expression) of Nox2 protein in brain
20) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.33 Pain Relevance 0.06

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