INT188852

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Context Info
Confidence 0.19
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 13
Total Number 26
Disease Relevance 6.44
Pain Relevance 5.35

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

cytosol (Pde2a) signal transduction (Pde2a) Golgi apparatus (Pde2a)
endoplasmic reticulum (Pde2a) plasma membrane (Pde2a) nucleus (Pde2a)
Anatomy Link Frequency
myocytes 5
spinal cord 3
cardiac myocytes 2
paw 1
endothelia 1
Pde2a (Mus musculus)
Pain Link Frequency Relevance Heat
Spinal cord 348 100.00 Very High Very High Very High
Morphine 192 100.00 Very High Very High Very High
Analgesic 36 100.00 Very High Very High Very High
Pain 132 99.68 Very High Very High Very High
allodynia 120 99.38 Very High Very High Very High
analgesia 24 98.76 Very High Very High Very High
Eae 72 95.00 High High
qutenza 12 92.24 High High
Inflammatory stimuli 12 88.60 High High
Dorsal horn 12 82.88 Quite High
Disease Link Frequency Relevance Heat
Nociception 300 100.00 Very High Very High Very High
Pain 156 99.68 Very High Very High Very High
Neuropathic Pain 132 99.38 Very High Very High Very High
Coronary Heart Disease 182 99.04 Very High Very High Very High
Natriuresis 70 97.96 Very High Very High Very High
Targeted Disruption 28 95.16 Very High Very High Very High
Inflammatory Pain 48 95.00 High High
Hypertrophy 56 90.96 High High
Sprains And Strains 48 89.72 High High
INFLAMMATION 36 88.24 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
At least two cGMP-stimulated proteins (as third messengers) are expressed in myocytes: PKG I; and phosphodiesterase (PDE) 2, a dual substrate esterase, which appears to hydrolyze cGMP under resting conditions [2], but targets cAMP in the presence of ?
Gene_expression (expressed) of cGMP in myocytes
1) Confidence 0.19 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.14 Pain Relevance 0
Novel insights into the mechanisms mediating the local antihypertrophic effects of cardiac atrial natriuretic peptide: role of cGMP-dependent protein kinase and RGS2

Cardiac atrial natriuretic peptide (ANP) locally counteracts cardiac hypertrophy via the guanylyl cyclase-A (GC-A) receptor and cGMP production, but the downstream signalling pathways are unknown.

Gene_expression (production) of cGMP associated with natriuresis and coronary heart disease
2) Confidence 0.19 Published 2010 Journal Basic Res Cardiol Section Title Doc Link PMC2916114 Disease Relevance 0.51 Pain Relevance 0
In conclusion, our observations support the notion that cGMP synthesized by sGC (in response to NO) and membrane-bound GC-A (in response to ANP) does not feed a common cGMP pool in cardiac myocytes, but instead remains spatially and functionally compartmentalized to modulate different targets and thereby different myocyte functions.


Gene_expression (synthesized) of cGMP in cardiac myocytes
3) Confidence 0.17 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.17 Pain Relevance 0
In contrast, nitric oxide (NO)-stimulated cGMP production in the cytosol (which is mediated by the soluble guanylyl cyclase, sGC), markedly blunted the cardiac contractile responses to ISO [44, 50].
Gene_expression (production) of cGMP
4) Confidence 0.17 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.28 Pain Relevance 0
Counteraction of the cardiac Ang II effects by ANP/GC-A/cGMP involves PKG I and RGS2
Gene_expression (/) of cGMP
5) Confidence 0.17 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.14 Pain Relevance 0
Counteraction of the cardiac Ang II effects by ANP/GC-A/cGMP involves PKG I and RGS2
Gene_expression (/) of cGMP
6) Confidence 0.17 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.14 Pain Relevance 0
Collectively, our findings are compatible with the notion that PKG I is the downstream target activated by the ANP/GC-A/cGMP-signalling pathway in cardiac myocytes. cGMP/PKG I-mediated modulation of RGS2 and subsequent inhibition of AT1/G?
Gene_expression (modulation) of cGMP in cardiac myocytes
7) Confidence 0.17 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0 Pain Relevance 0
Several cGMP-modulated proteins are expressed in myocytes, such as phosphodiesterases (PDE 2, 3 and 9) and PKG I [47].
Gene_expression (expressed) of PDE 2 in myocytes
8) Confidence 0.15 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0 Pain Relevance 0
This could be due to spatial compartmentalization or could be related to different concentrations of cGMP reached after GC-A stimulation in myocytes (expressing low levels of GC-A) when compared with endothelia (with very dense GC-A expression) [25, 26].
Gene_expression (expressing) of cGMP in endothelia
9) Confidence 0.15 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0 Pain Relevance 0
In conclusion, our observations support the notion that cGMP synthesized by sGC (in response to NO) and membrane-bound GC-A (in response to ANP) does not feed a common cGMP pool in cardiac myocytes, but instead remains spatially and functionally compartmentalized to modulate different targets and thereby different myocyte functions.


Gene_expression (pool) of cGMP in myocyte
10) Confidence 0.15 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.16 Pain Relevance 0
-adrenergic calcium and contractile responses of adult myocytes and intact hearts are unaffected by ANP/GC-A-elicited cGMP production at the plasma membrane.
Gene_expression (production) of cGMP in hearts
11) Confidence 0.15 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.27 Pain Relevance 0
At least two cGMP-stimulated proteins (as third messengers) are expressed in myocytes: PKG I; and phosphodiesterase (PDE) 2, a dual substrate esterase, which appears to hydrolyze cGMP under resting conditions [2], but targets cAMP in the presence of ?
Gene_expression (hydrolyze) of cGMP in myocytes
12) Confidence 0.15 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.13 Pain Relevance 0
Hence, these studies indicate that the NO/sGC/cGMP system acts as a negative modulator of both the cardiac contractile and hypertrophic responses to ?
Gene_expression (system) of cGMP
13) Confidence 0.15 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.19 Pain Relevance 0
Several cGMP-modulated proteins are expressed in myocytes, such as phosphodiesterases (PDE 2, 3 and 9) and PKG I [47].
Gene_expression (expressed) of cGMP in myocytes
14) Confidence 0.13 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0 Pain Relevance 0
However, our observations do support the hypothesis that within the spinal cord multi-level changes in CO/NO-cGMP system gene expression follow noxious stimulation.
Gene_expression (expression) of cGMP in spinal cord associated with spinal cord
15) Confidence 0.12 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.53 Pain Relevance 0.61
Basal expression of PDE2,3 and 5 has been demonstrated in spinal cord tissue [10,11].
Gene_expression (expression) of PDE2 in spinal cord associated with spinal cord
16) Confidence 0.11 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.48 Pain Relevance 0.58
One set of issues is: By what mechanism is the response of the CO/NO-cGMP signaling system coordinated?
Gene_expression (system) of cGMP
17) Confidence 0.11 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.44 Pain Relevance 0.27
Thus while the data pertaining to gene expression for some CO/NO-cGMP signaling system components and the large number of pharmacological studies not cited above support roles for this system in nociceptive signal transmission, few studies have attempted to follow the expression of the various components under standardized conditions.
Gene_expression (expression) of cGMP associated with nociception
18) Confidence 0.09 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.39 Pain Relevance 0.58
Thus it appears both that 1) the enhanced expression of CO/NO-cGMP system genes requires the intense acute nociception characteristic of formalin injection, and 2) that long term hind paw sensitisation does not require enhanced expression of these genes.
Gene_expression (expression) of cGMP in paw associated with nociception
19) Confidence 0.09 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.30 Pain Relevance 0.32
Once produced, these monoxides converge on guanylate cyclase to stimulate the production of cGMP.
Gene_expression (production) of cGMP
20) Confidence 0.09 Published 2005 Journal Mol Pain Section Body Doc Link PMC1310513 Disease Relevance 0.57 Pain Relevance 0.60

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