INT101983

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Context Info
Confidence 0.46
First Reported 2002
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 11
Total Number 12
Disease Relevance 6.01
Pain Relevance 4.99

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 (Ptgir) plasma membrane (Ptgir) signal transducer activity (Ptgir)
Anatomy Link Frequency
macrophages 1
spinal cord 1
platelet 1
PGE2 1
body 1
Ptgir (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 329 99.98 Very High Very High Very High
Spinal cord 7 99.50 Very High Very High Very High
Inflammation 123 99.40 Very High Very High Very High
Pain 78 98.86 Very High Very High Very High
ischemia 9 98.08 Very High Very High Very High
cOX1 7 95.88 Very High Very High Very High
antagonist 48 95.04 Very High Very High Very High
Hyperalgesia 21 94.32 High High
Thermal hyperalgesia 77 93.76 High High
agonist 28 92.64 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 23 99.76 Very High Very High Very High
Nociception 93 99.56 Very High Very High Very High
INFLAMMATION 150 99.40 Very High Very High Very High
Injury 14 99.36 Very High Very High Very High
Pain 89 98.86 Very High Very High Very High
Coronary Artery Disease 4 98.08 Very High Very High Very High
Cv Unclassified Under Development 5 94.44 High High
Hyperalgesia 98 94.32 High High
Lung Cancer 39 93.24 High High
Nicotine Addiction 2 88.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results suggest that PGI2 is involved in pain transmission at the spinal cord following expression of IP receptor mRNA induced by peripheral inflammation.
Positive_regulation (induced) of IP receptor mRNA in spinal cord associated with pain, inflammation and spinal cord
1) Confidence 0.46 Published 2002 Journal Neuroreport Section Abstract Doc Link 11924902 Disease Relevance 0.67 Pain Relevance 0.62
BACKGROUND/AIM: We investigated the role of prostacyclin (PGI2) IP receptors in the acid-induced secretion of HCO3- using IP receptor knockout [IP (-/-)] mice, in comparison with capsaicin-induced secretion.
Spec (investigated) Positive_regulation (role) of prostacyclin associated with targeted disruption and qutenza
2) Confidence 0.36 Published 2004 Journal Digestion Section Abstract Doc Link 15308871 Disease Relevance 0.10 Pain Relevance 0.17
However, increased PGI2 may also attenuate relief of pain.
Positive_regulation (increased) of PGI2 associated with pain
3) Confidence 0.20 Published 2008 Journal J. Intern. Med. Section Abstract Doc Link 18410593 Disease Relevance 1.30 Pain Relevance 0.54
Thus, the potentiation or sensitization of TRPV1 activity through EP1 or IP activation might be one important mechanism underlying the peripheral nociceptive actions of PGE2 or PGI2.



Positive_regulation (activation) of IP in PGE2 associated with nociception
4) Confidence 0.20 Published 2005 Journal Mol Pain Section Abstract Doc Link PMC1074353 Disease Relevance 0.56 Pain Relevance 0.28
The temperature threshold for TRPV1 activation was significantly reduced (from 38.2 ± 0.5°C, n = 5 to 32.2 ± 1.2°C, n = 5) in the presence of PGI2, suggesting the possibility that IP receptor activation can cause nociception at body temperature (Figure 5E).
Positive_regulation (activation) of IP in body associated with nociception
5) Confidence 0.18 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.39 Pain Relevance 0.41
However, more than micromolar-order concentrations of PGE2 and PGI2 have been reported to be synthesized by macrophages upon lipopolysacharide (LPS) stimulation [33,34], suggesting that 1 ?
Positive_regulation (concentrations) of PGI2 in macrophages
6) Confidence 0.17 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.75 Pain Relevance 0.44
This property might explain the dose-dependent effects of PGI2 on capsaicin-activated currents: PKC-dependent sensitization of TRPV1 occurs downstream of Gq-coupled IP receptor activation at high concentrations (1000 nM) of PGI2 (1.5 min) while long (6.5 min) treatment with low concentrations (100 nM) of PGI2 causes potentiation of TRPV1 activity through Gs activation.
Positive_regulation (activation) of IP associated with qutenza
7) Confidence 0.16 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.08 Pain Relevance 0.42
This property might explain the dose-dependent effects of PGI2 on capsaicin-activated currents: PKC-dependent sensitization of TRPV1 occurs downstream of Gq-coupled IP receptor activation at high concentrations (1000 nM) of PGI2 (1.5 min) while long (6.5 min) treatment with low concentrations (100 nM) of PGI2 causes potentiation of TRPV1 activity through Gs activation.
Positive_regulation (activation) of PGI2 associated with qutenza
8) Confidence 0.16 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.08 Pain Relevance 0.42
Indeed, injury-induced platelet activation is enhanced in PGI2 receptor (IP) knock-out mice [58], whereas it is reduced in TxA2 receptor (TP) knock-out mice [58].
Positive_regulation (enhanced) of PGI2 receptor in platelet associated with targeted disruption and injury
9) Confidence 0.14 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563450 Disease Relevance 0.95 Pain Relevance 0.51
PGI2 can signal through a specific cell surface receptor, designated IP, which is a
Positive_regulation (designated) of IP
10) Confidence 0.06 Published 2008 Journal PPAR Research Section Body Doc Link PMC2396386 Disease Relevance 0.61 Pain Relevance 0.04
Capsaicin increased mucosal PGI2 but not PGE2 levels, corroborating this observation that only PGI2 receptor knock-out mice abolished capsaicin induced HCO3- secretion.
Positive_regulation (increased) of PGI2 associated with targeted disruption and qutenza
11) Confidence 0.04 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.52 Pain Relevance 0.93
-galactosidase ipRGCs is dependent on the retinal ON-bipolar functional circuit, tau-lacZ+/+ animals were treated with L-AP4 prior to light stimulation.
Positive_regulation (dependent) of ipRGCs
12) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2655650 Disease Relevance 0 Pain Relevance 0.21

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