INT55879

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Context Info
Confidence 0.78
First Reported 1994
Last Reported 2011
Negated 2
Speculated 16
Reported most in Body
Documents 421
Total Number 440
Disease Relevance 240.74
Pain Relevance 166.02

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 (CCL2) extracellular space (CCL2) aging (CCL2)
extracellular region (CCL2) cell adhesion (CCL2) cytoskeleton organization (CCL2)
Anatomy Link Frequency
monocyte 81
macrophage 22
endothelial cells 20
plasma 17
microglia 15
CCL2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 5189 100.00 Very High Very High Very High
cytokine 4077 100.00 Very High Very High Very High
chemokine 3648 100.00 Very High Very High Very High
Inflammatory mediators 310 100.00 Very High Very High Very High
addiction 16 100.00 Very High Very High Very High
intrathecal 17 99.98 Very High Very High Very High
mu opioid receptor 8 99.96 Very High Very High Very High
Morphine 2498 99.92 Very High Very High Very High
Angina 191 99.92 Very High Very High Very High
acular 36 99.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 5894 100.00 Very High Very High Very High
Cancer 1397 100.00 Very High Very High Very High
Injury 898 100.00 Very High Very High Very High
Adhesions 755 100.00 Very High Very High Very High
Liver Disease 477 100.00 Very High Very High Very High
Necrosis 418 100.00 Very High Very High Very High
Viral Meningitis 213 100.00 Very High Very High Very High
Dengue 107 100.00 Very High Very High Very High
Primary Sclerosing Cholangitis 548 99.96 Very High Very High Very High
Syndrome 238 99.96 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results suggest that lidocaine may modulate MCP-1 production and MCP-1-induced activation in inflammatory cells.
Gene_expression (production) of MCP-1 associated with inflammation and lidocaine
1) Confidence 0.78 Published 2003 Journal Anesth. Analg. Section Abstract Doc Link 14570645 Disease Relevance 0.42 Pain Relevance 0.74
Lidocaine may modulate MCP-1-induced monocyte response, as reflected by chemotaxis, cytosolic-free calcium, and lipopolysaccharide-induced MCP-1 production by human monocytic THP-1 cells.
Gene_expression (production) of MCP-1 in THP-1 associated with lidocaine
2) Confidence 0.78 Published 2003 Journal Anesth. Analg. Section Abstract Doc Link 14570645 Disease Relevance 0.39 Pain Relevance 0.68
Lidocaine inhibited lipopolysaccharide-induced MCP-1 production as well as messenger RNA expression in a dose-dependent manner.
Gene_expression (production) of MCP-1 associated with lidocaine
3) Confidence 0.78 Published 2003 Journal Anesth. Analg. Section Abstract Doc Link 14570645 Disease Relevance 0.40 Pain Relevance 0.71
The purpose of this study was to explore the influence of morphine on CCL2 expression by human neurons.
Gene_expression (expression) of CCL2 in neurons associated with morphine
4) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0 Pain Relevance 1.17
Morphine has previously been shown to stimulate CCL2 expression in other cell types [5], and other investigators have shown that neurons constitutively express CCL2 [9-13].
Gene_expression (express) of CCL2 in neurons associated with morphine
5) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.07 Pain Relevance 0.98
However, this finding doe not preclude the involvement of DORs or of a non-opioid receptor mechanism in morphine-induced stimulation of CCL2 production.
Gene_expression (production) of CCL2 associated with opioid receptor and morphine
6) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.06 Pain Relevance 1.14
However, this study demonstrated for the first time that morphine can stimulate production of CCL2 by human neurons.
Gene_expression (production) of CCL2 in neurons associated with morphine
7) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.08 Pain Relevance 0.99
Morphine has previously been shown to stimulate CCL2 expression in other cell types [5], and other investigators have shown that neurons constitutively express CCL2 [9-13].
Gene_expression (expression) of CCL2 in neurons associated with morphine
8) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.06 Pain Relevance 0.97
However, one potential implication of the specificity for neurons of morphine's stimulatory effect on CCL2 production is that opiates may increase recruitment of inflammatory cells within the CNS via their effect on neurons.
Gene_expression (production) of CCL2 in neurons associated with inflammation, central nervous system, opiate and morphine
9) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.39 Pain Relevance 1.06
Taken together, the findings in this study support the hypothesis that morphine stimulates CCL2 expression by human neurons and add another mechanism to a growing repertoire whereby opiates could alter the neuroinflammatory process.


Gene_expression (expression) of CCL2 in neurons associated with opiate and morphine
10) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.47 Pain Relevance 0.72
In the course of testing the hypothesis that morphine would stimulate CCL2 production by neurons, three observations were made: 1) CCL2, which was the only chemokine examined that was constitutively expressed by neurons under our experimental conditions, was significantly upregulated in neurons by exposure to morphine; 2) morphine's enhancement of CCL2 was specific for neurons, as witnessed by a lack of response of astrocytes and microglia to morphine under our experimental conditions; and 3) morphine's potentiation of neuronal CCL2 production involves the MOR.
Gene_expression (production) of CCL2 in astrocytes associated with chemokine, opioid receptor and morphine
11) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.05 Pain Relevance 1.05
Generally, astrocytes and microglia have been regarded as the main brain cell sources of this important chemokine [7], and indeed we demonstrated that both glial cell populations do express CCL2 constitutively.
Gene_expression (express) of CCL2 in glial cell associated with chemokine
12) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0.09 Pain Relevance 1.04
In the course of testing the hypothesis that morphine would stimulate CCL2 production by neurons, three observations were made: 1) CCL2, which was the only chemokine examined that was constitutively expressed by neurons under our experimental conditions, was significantly upregulated in neurons by exposure to morphine; 2) morphine's enhancement of CCL2 was specific for neurons, as witnessed by a lack of response of astrocytes and microglia to morphine under our experimental conditions; and 3) morphine's potentiation of neuronal CCL2 production involves the MOR.
Gene_expression (production) of CCL2 in astrocytes associated with chemokine, opioid receptor and morphine
13) Confidence 0.78 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1712222 Disease Relevance 0 Pain Relevance 1.30
MCP-1, abundantly produced during gestation by
Gene_expression (produced) of MCP-1
14) Confidence 0.78 Published 2007 Journal Mediators of Inflammation Section Body Doc Link PMC2234089 Disease Relevance 0.32 Pain Relevance 0
hypertension, which is not associated with endothelial dysfunction [39] and thus, with probably higher MCP-1 production.
Gene_expression (production) of MCP-1 associated with hypertension
15) Confidence 0.78 Published 2007 Journal Mediators of Inflammation Section Body Doc Link PMC2234089 Disease Relevance 0.25 Pain Relevance 0
Importantly, increased glial expression of MOR can trigger an opiate-driven amplification/positive feedback of MCP-1 production and inflammation.
Gene_expression (production) of MCP-1 associated with inflammation, opiate and opioid receptor
16) Confidence 0.77 Published 2006 Journal Glia Section Abstract Doc Link 16206161 Disease Relevance 0.27 Pain Relevance 0.91
HIV-1 Tat and opiate-induced changes in astrocytes promote chemotaxis of microglia through the expression of MCP-1 and alternative chemokines.
Gene_expression (expression) of MCP-1 in microglia associated with chemokine and opiate
17) Confidence 0.77 Published 2006 Journal Glia Section Title Doc Link 16206161 Disease Relevance 0.71 Pain Relevance 0.87
Intrathecal synthesis of monocyte chemoattractant protein-1 (MCP-1) in amyotrophic lateral sclerosis: further evidence for microglial activation in neurodegeneration.
Gene_expression (synthesis) of MCP-1 in lateral associated with motor neuron diseases and intrathecal
18) Confidence 0.77 Published 2003 Journal J. Neuroimmunol. Section Title Doc Link 14597108 Disease Relevance 0.61 Pain Relevance 0.18
Intrathecal synthesis of monocyte chemoattractant protein-1 (MCP-1) in amyotrophic lateral sclerosis: further evidence for microglial activation in neurodegeneration.
Gene_expression (synthesis) of monocyte chemoattractant protein-1 in lateral associated with motor neuron diseases and intrathecal
19) Confidence 0.77 Published 2003 Journal J. Neuroimmunol. Section Title Doc Link 14597108 Disease Relevance 0.61 Pain Relevance 0.18
Enhanced MCP-1 expression has been detected in macrophages, endothelial cells, and vascular smooth muscle cells in the atheromatous plaque.
Gene_expression (expression) of MCP-1 in plaque
20) Confidence 0.75 Published 2002 Journal Clin Cardiol Section Abstract Doc Link 12000070 Disease Relevance 0.63 Pain Relevance 0.19

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