INT107674

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Context Info
Confidence 0.27
First Reported 2003
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 13
Disease Relevance 8.91
Pain Relevance 2.88

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

nucleoplasm (Parp1) nuclear envelope (Parp1) intracellular (Parp1)
DNA binding (Parp1) protein complex (Parp1) nucleolus (Parp1)
Anatomy Link Frequency
microglial cells 2
poly 1
nerve 1
cleavage 1
Parp1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
ischemia 350 99.78 Very High Very High Very High
diabetic neuropathy 10 99.32 Very High Very High Very High
sSRI 8 98.28 Very High Very High Very High
Brush evoked pain 80 97.76 Very High Very High Very High
Hyperalgesia 20 96.08 Very High Very High Very High
fluoxetine 1 83.36 Quite High
Inflammatory response 42 82.00 Quite High
depression 1 74.64 Quite High
Pain 17 72.32 Quite High
antidepressant 1 68.16 Quite High
Disease Link Frequency Relevance Heat
Cv Unclassified Under Development 322 99.78 Very High Very High Very High
Apoptosis 76 99.68 Very High Very High Very High
Diabetic Neuropathy 10 99.32 Very High Very High Very High
Stress 11 97.96 Very High Very High Very High
Neuropathic Pain 94 97.76 Very High Very High Very High
Hyperalgesia 20 96.08 Very High Very High Very High
Diabetes Mellitus 204 95.48 Very High Very High Very High
Epstein-barr Virus 6 93.96 High High
Brain Hemorrhage 21 93.88 High High
Ovarian Cancer 96 90.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In order to investigate the role of microglial cells in the stimulation of neuroplastic changes, PARP-1 inhibition was used as a means of down-regulating the microglial response induced by ischemia.
Negative_regulation (inhibition) of PARP-1 in microglial cells associated with ischemia
1) Confidence 0.27 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779656 Disease Relevance 0.38 Pain Relevance 0.11
Treatment with inhibitors of PARP-1, an enzyme sensitive to oxidative and nitrosative stress, normalizes deficits in nerve blood flow, conduction velocity, and energy metabolism in experimental diabetes but only partially ameliorates sensory nerve function (19–21).
Negative_regulation (inhibitors) of PARP-1 in nerve associated with stress and diabetes mellitus
2) Confidence 0.25 Published 2008 Journal Diabetes Section Body Doc Link PMC2551692 Disease Relevance 1.11 Pain Relevance 0.45
Consistent with a rapid PARP-1 activation described after focal ischemia [43], the PARP-1 inhibition was performed by 3-AB i.p. injection right after the induction of photothrombotic ischemia.
Negative_regulation (inhibition) of PARP-1 associated with ischemia
3) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779656 Disease Relevance 0.75 Pain Relevance 0.34
As a means of down-regulating the microglial response induced by ischemia, 3-aminobenzamide (3-AB, 90 mg/kg, i.p.) was used to inhibit the poly(ADP-ribose) polymerase-1 (PARP-1).
Negative_regulation (inhibit) of PARP-1 in poly associated with ischemia
4) Confidence 0.20 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2779656 Disease Relevance 0.55 Pain Relevance 0.20
Finally, a robust and important decrease of OX-42 and ED-1 staining was observed in 3-AB treated animals in the early phase of ischemia, confirming that PARP-1 inhibition is an efficient approach for the modulation of local resident microglial activation and proliferation.
Negative_regulation (inhibition) of PARP-1 associated with ischemia
5) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779656 Disease Relevance 0.48 Pain Relevance 0.19
These results showed that PARP-1 inhibition induces a robust decrease in resident microglial cells activation.
Negative_regulation (inhibition) of PARP-1 in microglial cells
6) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779656 Disease Relevance 0.41 Pain Relevance 0.17
Interestingly, despite the effective PARP-1 inhibition evidenced by a strong decrease in PAR staining, no significant differences in term of temporal evolution of lesion size between vehicle and 3-AB treated animals were observed.
Negative_regulation (inhibition) of PARP-1
7) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779656 Disease Relevance 0.63 Pain Relevance 0.26
In our experimental conditions, PARP-1 inhibition by 3-AB treatment was associated with a very important decrease in OX-42 staining at 4 h (Fig. 4B1–2) and 24 h (Fig. 4D1–2) of ischemia as compared to vehicle treated animals.
Negative_regulation (inhibition) of PARP-1 associated with ischemia
8) Confidence 0.20 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779656 Disease Relevance 0.38 Pain Relevance 0.15
This is consistent with our observation that the PARP-1 inhibitor PJ34 does not significantly prevent the development of tactile allodynia (Fig. 1B) or mechanical hyperalgesia (Table 3) in experimentally diabetic rats.
Negative_regulation (inhibitor) of PARP-1 associated with brush evoked pain, hyperalgesia and diabetes mellitus
9) Confidence 0.18 Published 2008 Journal Diabetes Section Body Doc Link PMC2551692 Disease Relevance 1.33 Pain Relevance 0.53
Treatment with 1.25 µM Fe-SP revealed a similar result, with some activation of caspase-9, and -3, and inactivation of PARP-1 while the activation of caspase-8 was as strong as observed for 2.5 µM Fe-SP.
Negative_regulation (inactivation) of PARP-1
10) Confidence 0.10 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386551 Disease Relevance 0.57 Pain Relevance 0
To define the cellular response of SKOV-3 cells upon Fe-SP treatment we analyzed the activation of caspases characteristic for induction of apoptosis as well as the inactivation of PARP-1 by immunoblotting.
Negative_regulation (inactivation) of PARP-1 associated with apoptosis
11) Confidence 0.10 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386551 Disease Relevance 0.53 Pain Relevance 0
Western blotting confirmed the activation of effector caspase-3 and inactivation of PARP-1 (involved in DNA repair) [24] during the execution of apoptosis in SKOV-3 cells following Fe-SP treatment.
Negative_regulation (inactivation) of PARP-1 associated with apoptosis
12) Confidence 0.10 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386551 Disease Relevance 0.88 Pain Relevance 0
Resultant SSRI-induced apoptosis was preceded by caspase activation, poly(ADP-ribose) polymerase-1 (PARP-1) cleavage, DNA fragmentation, a loss of mitochondrial membrane potential, and the externalization of phosphatidylserine, and reversed by the overexpression of bcl-2.
Negative_regulation (loss) of PARP-1 in cleavage associated with apoptosis and ssri
13) Confidence 0.08 Published 2003 Journal Blood Section Abstract Doc Link 12515726 Disease Relevance 0.91 Pain Relevance 0.47

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