INT250282

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.54
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 32
Total Number 33
Disease Relevance 32.96
Pain Relevance 9.07

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

transport (AQP4) plasma membrane (AQP4) transmembrane transport (AQP4)
cytoplasm (AQP4)
Anatomy Link Frequency
astrocyte 5
spinal cord 4
plasma 1
blood vessels 1
gray matter 1
AQP4 (Homo sapiens)
Pain Link Frequency Relevance Heat
Spinal cord 341 99.84 Very High Very High Very High
Central nervous system 303 99.46 Very High Very High Very High
Multiple sclerosis 210 99.24 Very High Very High Very High
Demyelination 78 99.24 Very High Very High Very High
dexamethasone 8 98.28 Very High Very High Very High
Glutamate 702 98.12 Very High Very High Very High
cerebral cortex 26 95.16 Very High Very High Very High
Inflammation 180 95.08 Very High Very High Very High
Neuritis 93 93.68 High High
Dopamine 104 91.72 High High
Disease Link Frequency Relevance Heat
Neuromyelitis Optica 2085 100.00 Very High Very High Very High
Targeted Disruption 184 99.88 Very High Very High Very High
Cerebral Amyloid Angiopathy 65 99.64 Very High Very High Very High
Creutzfeldt Jakob Disease 130 99.44 Very High Very High Very High
Necrosis 39 99.32 Very High Very High Very High
Demyelinating Disease 452 99.24 Very High Very High Very High
Lewy Body Disease 39 98.56 Very High Very High Very High
Disease 990 98.44 Very High Very High Very High
Pressure And Volume Under Development 28 97.52 Very High Very High Very High
Recurrence 328 97.48 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In this study, we demonstrate that: (a) when active complement is present, binding of NMO-IgG to AQP4 in astrocyte membranes causes membrane lesioning; (b) in the absence of complement, NMO-IgG causes antigen-specific removal of AQP4 from astrocytic membranes with reduction of Na+-dependent glutamate transport and loss of surface EAAT2; (c) transgenic expression of AQP4 in nonastrocytic cells, and physiological up-regulation of AQP4 in differentiating astrocytes, induces surface EAAT2 expression; (d) AQP4 and EAAT2 exist in astrocytic membranes as a macromolecular complex; and (e) regions of AQP4 loss in NMO spinal cord lesions are deficient in EAAT2.
Negative_regulation (loss) of AQP4 in astrocyte associated with targeted disruption, neuromyelitis optica, glutamate and spinal cord
1) Confidence 0.54 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.03 Pain Relevance 0.32
AQP4 loss at sites of C9neo deposition is a representative finding in our nine previously published cases (4).
Negative_regulation (loss) of AQP4
2) Confidence 0.54 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.88 Pain Relevance 0.50
Loss of AQP4 is a distinctive finding in both early and late lesions of NMO (4).
Negative_regulation (Loss) of AQP4 associated with neuromyelitis optica
3) Confidence 0.54 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.51 Pain Relevance 0.35
Characteristic CNS lesions exhibit selective depletion of AQP4, with and without associated myelin loss; focal vasculocentric deposits of IgG, IgM, and complement; prominent edema; and inflammation.
Negative_regulation (depletion) of AQP4 in CNS associated with pressure and volume under development, inflammation and central nervous system
4) Confidence 0.54 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 1.06 Pain Relevance 0.41
Lesioned NMO spinal cord gray matter contrasts to normal appearing gray matter by exhibiting markedly reduced EAAT2, in addition to AQP4 loss and deposition of complement activation products (Fig. 5 B).
Negative_regulation (loss) of AQP4 in gray matter associated with neuromyelitis optica and spinal cord
5) Confidence 0.54 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.69 Pain Relevance 0.44
The marked loss of EAAT2 described in this report parallels loss of AQP4 in lesioned NMO spinal cord tissue and contrasts with the increases in EAAT2 and AQP4 reported in both active and chronic MS lesions (20).
Negative_regulation (loss) of AQP4 in spinal cord associated with neuromyelitis optica, multiple sclerosis and spinal cord
6) Confidence 0.54 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.03 Pain Relevance 0.58
Depletion of AQP4 water channels in the plasma membrane would disrupt water homeostasis and promote edema.
Negative_regulation (Depletion) of AQP4 in plasma associated with pressure and volume under development
7) Confidence 0.47 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.84 Pain Relevance 0.55
In summary, the intriguing report by Roemer and colleagues [80], describing loss of AQP4 in the absence of demyelination or necrosis suggests that binding of antibody to AQP4 may be the initial pathogenic event in NMO lesions.
Negative_regulation (loss) of AQP4 associated with neuromyelitis optica, necrosis and demyelination
8) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.30 Pain Relevance 0.32
Also in the second, less frequent, lesion type AQP4 loss was associated with vasculocentric IgG and IgM deposits, complement activation, and tissue rarefaction, but there was no evidence of demyelination [80].
Negative_regulation (loss) of AQP4 associated with demyelination
9) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.21 Pain Relevance 0.36
Loss of AQP4 occurs in the context of vasculocentric immune complex deposition, active demyelination and vascular hyperplasia with hyalinization.
Negative_regulation (Loss) of AQP4 associated with demyelination, hyalinosis and hyperplasia
10) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.31 Pain Relevance 0.39
Misu and colleagues [65] conducted an immunohistochemical analysis that revealed loss of AQP4 in 90% of the acute and chronic NMO lesions, which were more pronounced in the active perivascular lesions where immunoglobulins and complements were deposited.
Negative_regulation (loss) of AQP4 associated with neuromyelitis optica
11) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.53 Pain Relevance 0.27
In a comparable study, Misu and colleagues [65] showed some NMO lesions in which myelinated fibers were relatively preserved despite the loss of AQP4 staining, suggesting that the loss of AQP4 did not reflect necrosis and cell loss.
Negative_regulation (loss) of AQP4 associated with necrosis and neuromyelitis optica
12) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.22 Pain Relevance 0.22
These findings suggested that AQP4 loss may be the initial event in NMO lesions.
Negative_regulation (loss) of AQP4 associated with neuromyelitis optica
13) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.11 Pain Relevance 0.18
In rat muscles with experimental denervation, Jimi and colleagues [43] observed a remarkable and rapid decrease in AQP4 at the mRNA and protein levels confirmed by immunohistochemical findings that reveal a decreased AQP4 staining on the surface of myofibers.
Negative_regulation (decrease) of AQP4 in muscles
14) Confidence 0.46 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.12 Pain Relevance 0.03
Detection of NMO-IgG or AQP4 autoantibodies is clinically useful for early diagnosis of NMO and its related spectrum disorders (NMOSD), including single attack or recurrent LETM without ON, and recurrent ON without ATM; and especially early distinction between NMOSD and CMS [3].
Negative_regulation (Detection) of AQP4 associated with neuromyelitis optica, multiple sclerosis, transverse myelitis, demyelinating disease and neuritis
15) Confidence 0.42 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2941752 Disease Relevance 2.36 Pain Relevance 0.65
Serum containing NMO-IgG, but not control serum, induced rapid down-regulation of surface AQP4 (Fig. 1 A).
Negative_regulation (regulation) of AQP4 associated with neuromyelitis optica
16) Confidence 0.39 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.02 Pain Relevance 0.20
NMO spinal cord lesions lack both AQP4 and EAAT2
Negative_regulation (lack) of AQP4 in spinal cord associated with neuromyelitis optica and spinal cord
17) Confidence 0.39 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.50 Pain Relevance 0.35
Marked reduction of EAAT2 in AQP4-deficient regions of NMO patient spinal cord lesions supports our immunocytochemical and immunoprecipitation data.
Negative_regulation (reduction) of AQP4 in spinal cord associated with neuromyelitis optica and spinal cord
18) Confidence 0.39 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 0.96 Pain Relevance 0.40
Our observations in primary astrocytes, type 2 differentiated CG-4 cells, and transfected nonneural HEK-293 cells indicate that the interaction of NMO-IgG with AQP4 induces at least three possible outcomes, each potentially pathogenic: (a) complement activation, (b) down-regulation of AQP4, and (c) coupled down-regulation of the EAAT2 glutamate transporter.
Negative_regulation (regulation) of AQP4 in astrocytes associated with neuromyelitis optica and glutamate
19) Confidence 0.39 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.33 Pain Relevance 0.28
In AQP4 knock-out mice, the lack of AQP4 is mirrored by tight junction opening in brain microvessels, swelling of perivascular astrocytic processes, and BBB hyperpermeability [38].
Negative_regulation (lack) of AQP4 in brain associated with targeted disruption and pressure and volume under development
20) Confidence 0.39 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2945323 Disease Relevance 0.82 Pain Relevance 0.23

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox